2007 First Aid Ch 05 Immunology

Front 1

Young child presents with tetany
and candidiasis. Hypocalcemia
and immunosuppression are
ound.

Back 1

T cell deficient
(DiGeorge).

Front 2

Young child has recurrent lung
infections and granulomatous
lesions. What is the defect in
neutrophils?

Back 2

NADPH oxidase (chronic
granulomatous disease).

Front 3

A 2° lymphoid organ that has many afferents, 1 or more efferents. Encapsulated, with trabeculae.

Back 3

Lymph node

Front 4

Lymph node definition

Back 4

A 2° lymphoid organ that has many afferents, 1 or more efferents. Encapsulated, with trabeculae.

Front 5

Lymph node

function

Back 5

Functions are nonspecific filtration by macrophages, storage/proliferation
of B and T cells, antibody production.

Front 6

Lymph node
Follicle

what and location

Back 6

Site of B-cell localization and
proliferation. In outer cortex.

Front 7

Lymph node
Follicle

1° vs 2°

Back 7

1° follicles are dense and
dormant. 2° follicles have
pale central germinal
centers and are active.

Front 8

Lymph node
Medulla description

Back 8

Consists of medullary cords
(closely packed lymphocytes
and plasma cells) and
medullary sinuses.

Front 9

Lymph node
Medullary sinuses

Back 9

communicate with efferent
lymphatics and contain
reticular cells and macrophages.

Front 10

Lymph node
Paracortex description (cells, location, vessels)

Back 10

Houses T cells. Region of cortex between follicles and medulla. Contains high endothelial venules through which T and B cells enter from blood.

Front 11

Lymph node
Paracortex wrt extreme

Back 11

In an extreme cellular immune response,paracortex becomes greatly enlarged.

Front 12

Lymph node

which part is not well developed in patients with DiGeorge syndrome.

Back 12

Paracortex

Front 13

Lymph drainage

ducts

Back 13

Right lymphatic duct Drains right arm and right half of head.

Thoracic duct Drains everything else.

Front 14

Sinusoids of spleen description

Back 14

Long, vascular channels in red pulp with fenestrated “barrel hoop” basement membrane. Macrophages found nearby.

Front 15

Long, vascular channels in red pulp with fenestrated “barrel hoop” basement membrane. Macrophages found nearby.

Back 15

Sinusoids of spleen

Front 16

spleen

where are T cells

Back 16

in the periarterial lymphatic sheath (PALS) and in the red pulp
of the spleen.

Front 17

spleen

where are B cells

Back 17

B cells are found in follicles within the white pulp of the spleen.

Front 18

Site of T-cell differentiation and maturation.

Back 18

Thymus

Front 19

Thymus derivation

Back 19

From epithelium of 3rd branchial
pouches. Lymphocytes of mesenchymal origin.

Front 20

Thymus WRT capsule

Back 20

Encapsulated.

Front 21

Thymus

different areas and what happens there

Back 21

Cortex is dense with immature T cells;

medulla is pale with mature T cells and epithelial reticular cells and contains Hassall’s corpuscles.

Positive (MHC restriction) and negative selection
selection (nonreactive to self) occur at the
corticomedullary junction.

Front 22

where are Hassall’s corpuscles.

Back 22

Thymus medulla is pale with mature T cells and epithelial
reticular cells and contains Hassall’s corpuscles.

Front 23

what are Hassall’s corpuscles.

Back 23

formed from type VI epithelial reticular cells with unclear function

Front 24

1° Lymph node draining

Upper limb and lateral breast

Back 24

Axillary

Front 25

1° Lymph node draining

Stomach

Back 25

Celiac

Front 26

1° Lymph node draining

Duodenum and jejunum

Back 26

Superior mesenteric

Front 27

1° Lymph node draining

Sigmoid colon

Back 27

colic to the inferior mesenteric

Front 28

1° Lymph node draining

lower rectum and anal canal above pectinate line

Back 28

internal iliac

Front 29

1° Lymph node draining

anal canal below pectinate line

Back 29

superficial inguinal

Front 30

1° Lymph node draining

testies

Back 30

superficial and deep plexuses to the para-aortic

Front 31

1° Lymph node draining

scrotum

Back 31

superficial inguinal

Front 32

1° Lymph node draining

superficial thigh

Back 32

superficial inguinal

Front 33

1° Lymph node draining

lateral side of the dorsum of the foot

Back 33

popliteal

Front 34

Innate vs. adaptive immunity

Innate cells

Back 34

Consists of neutrophils, macrophages, dendritic cells, and complement.

Front 35

Innate vs. adaptive immunity

adaptive cells

Back 35

Consists of T cells, B cells,
and circulating antibody.

Front 36

Innate vs. adaptive immunity

innate receptor

Back 36

receptors that recognize pathogens are germline encoded

Front 37

Innate vs. adaptive immunity

adaptive receptor

Back 37

receptors that recognize pathogens undergo VDJ recombination during lymphocyte development

Front 38

Th1 cells produce/activate

Back 38

IL-2 and IFN-γ, activate macrophages and cytotoxic (CD8+) T cells.

Front 39

Th2 cells produce/activate

Back 39

IL-4, and IL-5; provide help for B cells to make antibody.

Front 40

produce IL-2 and IFN-γ, activate macrophages and cytotoxic (CD8+) T cells.

Back 40

Th1 cells

Front 41

produce IL-4, and IL-5; provide help for B cells to make antibody.

Back 41

Th2 cells

Front 42

MHC what is it and what encodes it

Back 42

major histocompatability complex, encoded by Human Leukocyte
Antigen (HLA) genes.

Front 43

MHC I

what HLA's

Back 43

HLA-A, HLA-B, HLA-C.

Front 44

MHC I

what cells

Back 44

Expressed on almost all nucleated cells.

Front 45

MHC I

what is antigen loaded in

Back 45

RER of mostly intracellular peptides.

Front 46

MHC I

mediation

Back 46

Mediates viral immunity.

Front 47

MHC I

pairing

Back 47

Pairs with β2-microglobulin.

Front 48

Pairs with β -microglobulin.

Back 48

MHC I

Front 49

MHC II

what HLA's

Back 49

HLA-DR, HLA-DP, HLA-DQ.

Front 50

MHC II

what cells

Back 50

Expressed only on antigen presenting cells (APCs).

Front 51

MHC II

what is antigen loaded in

Back 51

Antigen is loaded in an acidified endosome.

Front 52

Which MHC type

HLA-A, HLA-B, HLA-C.

Back 52

MHC I

Front 53

Which MHC type

Expressed on almost all nucleated cells.

Back 53

MHC I

Front 54

Which MHC type

Antigen is loaded in RER of mostly intracellular peptides.

Back 54

MHC I

Front 55

Which MHC type

Mediates viral immunity.

Back 55

MHC I

Front 56

Which MHC type

HLA-DR, HLA-DP, HLA-DQ.

Back 56

MHC II

Front 57

Which MHC type

Expressed only on antigen presenting cells (APCs).

Back 57

MHC II

Front 58

Which MHC type

Antigen is loaded in an acidified endosome.

Back 58

MHC II

Front 59

Which MHC type

Main determinants of organ rejection.

Back 59

MHC II

Front 60

Which lymphocyte B or T

Allergy (type I hypersensitivity)

Back 60

B : IgE

Front 61

Which lymphocyte B or T

Allergy (type IV hypersensitivity)

Back 61

T cells

Front 62

Major function of

CD4+ T cells

Back 62

help B cells make antibody and produce γ-interferon that activates macrophages.

Front 63

Major function of

CD8+ T cells

Back 63

Kill virus-infected cells directly

Front 64

B vs T cell role in organ rejection

Back 64

B cells--hyperacute (IgG)

T cells---Organ rejection (slow)

Front 65

T-cell glycoproteins
functions on just helper T

Back 65

Helper T cells have CD4, which binds to MHC II on antigen-presenting cells.

Front 66

T-cell glycoproteins
functions on just Cytotoxic T

Back 66

Cytotoxic T cells
have CD8, which binds to MHC I on virus- infected cells.

Front 67

T-cell glycoproteins
functions on both

Back 67

CD3 complex––cluster of
polypeptides associated with
a T-cell receptor. Important
in signal transduction.

Front 68

name the Antigen-presenting cells:

Back 68

1. Macrophage
2. B cell
3. Dendritic cell/langerhan's in skin

Front 69

# of signals are required for T cell activation

Back 69

2

Front 70

Th activation steps

Back 70

1. Foreign body is phagocytosed by APC
2. Foreign antigen is presented on MHC II and
recognized by TCR on Th cell (Signal 1).
3. “Costimulatory signal” is given by interaction
of B7 and CD28 (Signal 2).
4. Th cell activated to produce cytokines.

Front 71

Tc activation

Back 71

1. Endogenously synthesized (viral or self) proteins are presented on MHC I and
recognized by TCR on Tc cell (Signal 1).
2. IL-2 from Th cell activates Tc cell to kill virus-infected cell (Signal 2).

Front 72

Antibodies

function of Variable part of L and H chains

Back 72

recognizes antigens

Front 73

Antibodies

what fixes complement

Back 73

Constant part of H chain of IgM and IgG fixes complement.

Front 74

Fc and Fab fractions. what contributes

Back 74

Heavy chain contributes to Fc and Fab fractions. Light chain contributes only to Fab fraction.

Front 75

Fc and Fab

mnemonic

Back 75

Fab: antigen binding fragment

Fc:
Constant
Carboxy terminal
Complement-binding
(IgG + IgM only)
Carbohydrate
side chains
Complement binding
fragment

Front 76

Antibody diversity is generated by: (4 things)

Back 76

1. Random “recombination” of VJ (light-chain) or VDJ (heavy-chain) genes
2. Random combination of heavy chains with light chains
3. Somatic hypermutation
4. Addition of nucleotides to DNA during “genetic recombination” by terminal deoxynucleotidyl transferase

Front 77

describe in general

Opsonization

Back 77

Antibody promotes
phagocytosis

Front 78

describe in general

Neutralization

Back 78

Antibody prevents bacterial adherence

Front 79

describe in general

Complement activation

Back 79

Antibody activates complement, enhancing opsonization and lysis

Front 80

Antibody activates complement, enhancing opsonization and lysis

Back 80

Complement activation

Front 81

Antibody prevents bacterial adherence

Back 81

Neutralization

Front 82

Antibody promotes
phagocytosis

Back 82

Opsonization

Front 83

Immunoglobulin isotypes

Mature B lymphocytes express on their surfaces

Back 83

IgM and IgD

Front 84

Immunoglobulin isotypes

isotype switching mediated by

Back 84

by cytokines and CD40 ligand

Front 85

Immunoglobulin isotypes

plasma cells secrete

Back 85

IgA, IgE, or IgG.

Front 86

Immunoglobulin isotypes

IgG (what response, how common, where it goes, what it does)

Back 86

Main antibody in 2° response. Most abundant. Fixes complement, crosses the placenta,
opsonizes bacteria, neutralizes bacterial toxins and viruses.

Front 87

Immunoglobulin isotypes

Main antibody in 2° response.

Back 87

IgG

Front 88

Immunoglobulin isotypes

Most abundant.

Back 88

IgG

Front 89

Immunoglobulin isotypes

crosses the placenta

Back 89

IgG

Front 90

Immunoglobulin isotypes

Fixes complement, crosses the placenta, opsonizes bacteria, neutralizes bacterial toxins and viruses

Back 90

Fixes complement

Front 91

Immunoglobulin isotypes

IgA (what response, where it goes, structure elements, what it does)

Back 91

Prevents attachment of bacteria and viruses to mucous membranes, does not fix
complement. Monomer or dimer. Found in secretions. Picks up secretory component from epithelial cells before secretion.

Front 92

Immunoglobulin isotypes

IgA wrt complement

Back 92

does not fix
complement

Front 93

Immunoglobulin isotypes

Prevents attachment of bacteria and viruses to mucous membranes

Back 93

IgA

Front 94

Immunoglobulin isotypes

Monomer or dimer. Found in secretions

Back 94

IgA

Front 95

Immunoglobulin isotypes

Picks up secretory component
from epithelial cells before secretion.

Back 95

IgA

Front 96

Immunoglobulin isotypes

what are they

Back 96

IgG
IgA
IgM
IgD
IgE

Front 97

Immunoglobulin isotypes

IgM (when, what it does, where it goes, srtucture)

Back 97

Produced in the 1° response to an antigen. Fixes complement but does not cross the placenta. Antigen receptor on the surface of B cells. Monomer or pentamer.

Front 98

Immunoglobulin isotypes

Monomer or pentamer.

Back 98

IgM

Front 99

Immunoglobulin isotypes

Antigen receptor on the surface of B cells.

Back 99

IgM

Front 100

Immunoglobulin isotypes

Fixes complement but does not cross the placenta.

Back 100

IgM

Front 101

Immunoglobulin isotypes

IgD (what it does, where is it)

Back 101

Unclear function. Found on the surface of many B cells and in serum.

Front 102

Immunoglobulin isotypes

Unclear function. Found on the surface of many B cells and in serum.

Back 102

IgD

Front 103

Immunoglobulin isotypes

IgE (role, where, how common)

Back 103

Mediates immediate (type I) hypersensitivity Mediates immunity to worms.
Lowest concentration in serum.

Front 104

Immunoglobulin isotypes

Mediates immediate (type I) hypersensitivity by inducing the release of mediators from
mast cells and basophils when exposed to allergen.

Back 104

IgE

Front 105

Immunoglobulin isotypes

Mediates immunity to worms.

Back 105

IgE

Front 106

Immunoglobulin isotypes

Lowest concentration in serum.

Back 106

IgE

Front 107

Immunoglobulin isotypes

IgE (role in hypersensitivity mech)

Back 107

by inducing the release of mediators from mast cells and basophils when exposed to allergen.

Front 108

Ig epitopes

Allotype

Back 108

Allotype (polymorphism)––Ig epitope that differs among members of same species. Can be on light chain or heavy chain.

Front 109

Ig epitopes

Isotype

Back 109

iso (same). Common to same class.

Isotype (IgG, IgA, etc.)––Ig epitope common to a
single class of Ig (5 classes, determined by heavy
chain).

Front 110

Ig epitopes

Idiotype

Back 110

idio (unique). Hypervariable region is unique.

Idiotype (specific for a given antigen)––Ig epitope
determined by antigen-binding site.

Front 111

Ig epitope that differs
among members of same species. Can be on
light chain or heavy chain.

Back 111

Allotype (polymorphism)––

Front 112

Ig epitope common to a
single class of Ig (5 classes, determined by heavy
chain).

Back 112

Isotype (IgG, IgA, etc.)––

Front 113

(specific for a given antigen)––Ig epitope
determined by antigen-binding site.

Back 113

Idiotype

Front 114

Important cytokines

mnemonic

Back 114

“Hot T-bone stEAk”:
IL-1: fever (hot)
IL-2: stimulates T cells
IL-3: stimulates bone marrow
IL-4: stimulates IgE
production
IL-5: stimulates IgA
production

Front 115

what secretes and what is the role of

IL-1

Back 115

Secreted by macrophages. Stimulates T cells, B cells,
neutrophils, fibroblasts, and epithelial cells to
grow, differentiate, or synthesize specific products.
An endogenous pyrogen.

Front 116

what secretes and what is the role of

IL-2

Back 116

Secreted by Th cells. Stimulates growth of helper
and cytotoxic T cells.

Front 117

what secretes and what is the role of

IL-3

Back 117

Secreted by activated T cells. Supports the growth and differentiation of bone marrow stem cells. Has a function similar to GM-CSF.

Front 118

what secretes and what is the role of

IL-4

Back 118

Secreted by Th2 cells. Promotes growth of B cells. Enhances class switching of IgE and IgG.

Front 119

what secretes and what is the role of

IL-5

Back 119

Secreted by Th2 cells. Promotes differentiation of B
cells. Enhances class switching of IgA. Stimulates
production and activation of eosinophils.

Front 120

what secretes and what is the role of

IL-6

Back 120

Secreted by Th cells and macrophages. Stimulates
production of acute-phase reactants and immunoglobulins.

Front 121

what secretes and what is the role of

IL-8

Back 121

Major chemotactic factor for neutrophils.

Front 122

what secretes and what is the role of

IL-10

Back 122

Secreted by Th2 cells. Stimulates Th2 while
inhibiting Th1.

Front 123

what secretes and what is the role of

IL-12

Back 123

Secreted by B cells and macrophages. Activates NK
and Th1 cells.

Front 124

what secretes and what is the role of

gamma-interferon

Back 124

Secreted by Th1 cells. Stimulates macrophages.

Front 125

what secretes and what is the role of

TNF-α

Back 125

Secreted by macrophages. IL-2 receptor synthesis by Th cells. ↑ B-cell proliferation. Attracts and activates neutrophils. Stimulates dendritic cell migration to lymph nodes.

Front 126

Name the cytokine

An endogenous pyrogen.

Back 126

IL-1

Front 127

Name the cytokine

Secreted by macrophages. Stimulates T cells, B cells,
neutrophils, fibroblasts, and epithelial cells to
grow, differentiate, or synthesize specific products.

Back 127

IL-1

Front 128

Name the cytokine

Secreted by Th cells. Stimulates growth of helper
and cytotoxic T cells.

Back 128

IL-2

Front 129

Name the cytokine

Secreted by activated T cells. Supports the growth and differentiation of bone marrow stem cells.

Back 129

IL-3

Front 130

Name the cytokine

Has a function similar to GM-CSF.

Back 130

IL-3

Front 131

Name the cytokine

Secreted by Th2 cells. Promotes growth of B cells.
Enhances class switching of IgE and IgG.

Back 131

IL-4

Front 132

Name the cytokine

Secreted by Th2 cells. Promotes differentiation of B
cells. Enhances class switching of IgA.

Back 132

IL-5

Front 133

Name the cytokine

Stimulates production and activation of eosinophils.

Back 133

IL-5

Front 134

Name the cytokine

Secreted by Th cells and macrophages. Stimulates
production of acute-phase reactants and immunoglobulins.

Back 134

IL-6

Front 135

Name the cytokine

Major chemotactic factor for neutrophils.

Back 135

IL-8

Front 136

Name the cytokine

Secreted by Th2 cells. Stimulates Th2 while inhibiting Th1.

Back 136

IL-10

Front 137

Name the cytokine

Secreted by B cells and macrophages. Activates NK and Th1 cells.

Back 137

IL-12

Front 138

Name the cytokine

Secreted by Th1 cells. Stimulates macrophages.

Back 138

γ-interferon

Front 139

Name the cytokine

Secreted by macrophages. ↑ IL-2 receptor synthesis
by Th cells. ↑ B-cell proliferation.

Back 139

TNF-α

Front 140

Name the cytokine

Attracts and activates neutrophils. Stimulates dendritic cell migration to lymph nodes.

Back 140

TNF-α

Front 141

Cell surface proteins

Helper T cells

Back 141

CD4, TCR, CD3, CD28, CD40L.

Front 142

Cell surface proteins

Cytotoxic T cells

Back 142

CD8, TCR, CD3.

Front 143

Cell surface proteins

B cells

Back 143

IgM, B7, CD19, CD20, CD40, MHC II.

Front 144

Cell surface proteins

Macrophages

Back 144

MHC II, CD14. Receptors for Fc and C3b.

Front 145

Cell surface proteins

NK cells

Back 145

Receptors for MHC I, CD16, CD56.

Front 146

Cell surface proteins

All cells except mature red cells

Back 146

MHC I.

Front 147

what cell has

CD4

Back 147

Helper T cells

Front 148

what cell has

TCR

Back 148

Helper T cells
and
Cytotoxic T cells

Front 149

what cell has

CD3

Back 149

Helper T cells
and
Cytotoxic T cells

Front 150

what cell has

CD28

Back 150

Helper T cells

Front 151

what cell has

CD40L

Back 151

Helper T cells

Front 152

what cell has

CD8

Back 152

Cytotoxic T cells

Front 153

what cell has

IgM

Back 153

B cells

Front 154

what cell has

B7

Back 154

B cells

Front 155

what cell has

CD19

Back 155

B cells

Front 156

what cell has

CD20

Back 156

B cells

Front 157

what cell has

CD40

Back 157

B cells

Front 158

what cell has

MHC II

Back 158

APC's

Front 159

what cell has

Fc receptor (FcR)

Back 159

Dendritic cells

Macrophages

Front 160

what cell has

MHC I.

Back 160

All cells except mature red cells

Front 161

what cell has

CD14. Receptors for C3b

Back 161

Macrophages

Front 162

what cell has

Receptors for C3b

Back 162

Macrophages

Front 163

what cell has

Receptors for MHC I

Back 163

NK cells

Front 164

what cell has

CD16

Back 164

NK cells

Front 165

what cell has

CD56.

Back 165

NK cells

Front 166

Membrane attack complex of complement defends
against

Back 166

gram-negative bacteria. Activated by IgG

Front 167

Membrane attache complex

activation in general

Back 167

Activated by IgG or IgM in the classic pathway, (GM makes classic cars.)

Activated by molecules on the surface of microbes especially
endotoxin) in the alternate pathway.

Front 168

the two primary opsonins in
bacterial defense.

Back 168

C3b and IgG

Front 169

C3b and IgG are the

Back 169

two primary opsonins in
bacterial defense.

Front 170

Roles of different complement molecules

C1

Back 170

C1, C2, C3, C4––viral
neutralization.

Front 171

Roles of different complement molecules

C2

Back 171

C1, C2, C3, C4––viral
neutralization.

Front 172

Roles of different complement molecules

C3

Back 172

C1, C2, C3, C4––viral
neutralization.

Front 173

Roles of different complement molecules

C4

Back 173

C1, C2, C3, C4––viral
neutralization.

Front 174

Roles of different complement molecules

C3b

Back 174

C3b - opsonization.

Front 175

Roles of different complement molecules

C3a

Back 175

C3a, C5a––anaphylaxis.

Front 176

Roles of different complement molecules

C5a

Back 176

C3a, and C5a––anaphylaxis.

C5a––neutrophil chemotaxis.

Front 177

Roles of different complement molecules

C5b-9

Back 177

C5b-9––cytolysis by membrane
attack complex (MAC).

Front 178

Roles of different complement molecules

Deficiency of C1 esterase
inhibitor

Back 178

hereditary angioedema (overactive complement).

Front 179

Roles of different complement molecules

Deficiency of C3

Back 179

severe, recurrent pyogenic
sinus and respiratory tract
infections.

Front 180

Roles of different complement molecules

Deficiency of C6–C8

Back 180

Neisseria bacteremia.

Front 181

Roles of different complement molecules

Deficiency of decay
accelerating factor (DAF)

Back 181

leads to paroxysmal nocturnal
hemoglobinuria (PNH).

Front 182

Name the complement molecules involved in/function

viral neutralization.

Back 182

C1, C2, C3, C4

Front 183

Name the complement molecules involved in/function

opsonization.

Back 183

C3b

Front 184

Name the complement molecules involved in/function

anaphylaxis.

Back 184

C3a, C5a

Front 185

Name the complement molecules involved in/function

neutrophil chemotaxis.

Back 185

C5a

Front 186

Name the complement molecules involved in/function

cytolysis by membrane attack complex (MAC).

Back 186

C5b-9

Front 187

WRT complement
What leads to hereditary
angioedema

Back 187

Deficiency of C1 esterase
inhibitor

Front 188

WRT complement
What leads to severe, recurrent pyogenic sinus and respiratory tract infections.

Back 188

Deficiency of C3

Front 189

WRT complement
What leads to
Neisseria bacteremia.

Back 189

Deficiency of C6–C8

Front 190

WRT complement
What leads to paroxysmal nocturnal
hemoglobinuria (PNH).

Back 190

Deficiency of decay-
accelerating factor (DAF)

Front 191

hereditary angioedema aka

Back 191

overactive complement

Front 192

overactive complement aka

Back 192

hereditary angioedema

Front 193

proteins that place uninfected cells in an antiviral state.

Back 193

Interferons (α, β, γ) are

Front 194

Interferon mechanism

in general

Back 194

Interferons induce the production of a 2nd protein that inhibits viral protein synthesis by degrading viral mRNA (but not host mRNA).

Front 195

role of the interferons and what different ones do

Back 195

1. α- and β-interferons inhibit viral protein synthesis
2. γ-interferons ↑ MHC I
and II expression and
antigen presentation
in all cells
3. Activates NK cells to
kill virus-infected cells

Front 196

when are some of the times patients given preformed antibodies

Back 196

(passive)––To Be Healed
Rapidly.
After exposure to Tetanus toxin, Botulinum toxin, HBV, or Rabies,

Front 197

Antigen variation examples

wrt Bacteria

Back 197

Salmonella (two flagellar variants), Borrelia (relapsing fever), Neisseria gonorrhoeae
(pilus protein).

Front 198

Antigen variation examples

wrt Virus

Back 198

influenza (major = shift, minor = drift).

Front 199

Antigen variation examples

wrt Parasites

Back 199

trypanosomes (programmed
rearrangement).

Front 200

Antigen variation

wrt influenza major shift

Back 200

and RNA segment rearrangement

Front 201

Anergy describe in different cells

Back 201

Self-reactive T cells become nonreactive without costimulatory molecule.
B cells also become anergic, but tolerance is less complete than in T cells.

Front 202

Self-reactive T cells become nonreactive without costimulatory molecule.

Back 202

Anergy

Front 203

Hypersensitivity Mechs

Type I

Back 203

Anaphylactic and atopic: antigen cross-links IgE on presensitized mast cells and basophils, triggering
release of vasoactive amines (i.e., histamine).

Front 204

Hypersensitivity Mechs

Type II

Back 204

Antibody mediated– –IgM, IgG bind to antigen on “enemy”cell, leading to lysis (by complement)
or phagocytosis.

Front 205

Hypersensitivity Mechs

Type III

Back 205

Immune complex: antigen-antibody complexes activate complement, which attracts neutrophils;
neutrophils release lysosomal enzymes.

Front 206

Hypersensitivity Mechs

Type IV

Back 206

Delayed (T-cell-mediated): sensitized T cells encounter antigen and then release
lymphokines (leads to macrophage activation).

Front 207

Serum sickness

mech

Back 207

antibodies to the foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes
where they fix complement (leads to tissue damage).

Front 208

Arthus reaction

mech

Back 208

Intradermal injection of antigen induces antibodies, which form antigen-antibody complexes in the skin.
Characterized by edema, necrosis, and activation
of complement.

Front 209

Intradermal injection of antigen induces antibodies, which form antigen-antibody complexes in the skin.
Characterized by edema, necrosis, and activation
of complement.

Back 209

Arthus reaction

Front 210

antibodies to the foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes
where they fix complement (leads to tissue damage).

Back 210

Serum sickness

Front 211

which is more common

serum sickness or Arthus reaction

Back 211

Serum sickness

Front 212

which Hypersensitivity reactions are antibody mediated

Back 212

Types I, II, and III are all
antibody mediated.

Front 213

Hypersensitivity

why is Type 1 so fast

Back 213

Reaction develops rapidly after antigen exposure due to preformed antibody.

Front 214

Hypersensitivity

how does type II do its damage

Back 214

Cy-2-toxic.
Antibody and complement lead
to membrane attack complex
(MAC).

Front 215

serum sickness

cause and findings

Back 215

Most serum sickness is now
caused by drugs (not serum).

Fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5–10 days after antigen exposure.

Front 216

Fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5–10 days after antigen exposure.

Back 216

serum sickness

Front 217

Mnemonic for type III Hypersensitivity

Back 217

Imagine an immune complex as
3 things stuck together:
antigen-antibody-complement.

Front 218

is Type IV Hypersensitivity transferable by serum

Back 218

Cell mediated; therefore, it is
not transferable by serum.

Front 219

Type IV Hypersensitivity
mnemonic

Back 219

4 T’s = T lymphocytes,
Transplant rejections,
TB skin tests, Touching
(contact dermatitis).

Front 220

Hypersensitivity mnemonic

Back 220

ACID:
-Anaphylactic and Atopic
(type I)

-Cytotoxic (antibody mediated)
(type II)

-Immune complex (type III)

-Delayed (cell mediated)
(type IV)

Front 221

Diseases caused by hypersensitivity

Type I

Back 221

Anaphylaxis
Allergic rhinitis (hay fever)

Front 222

Diseases caused by hypersensitivity

Anaphylaxis

Back 222

Type I

Front 223

Diseases caused by hypersensitivity

Allergic rhinitis (hay fever)

Back 223

Type I

Front 224

Diseases caused by hypersensitivity

Type II

Back 224

Hemolytic anemia
Idiopathic thrombocytopenic purpura
Erythroblastosis fetalis
Rheumatic fever
Goodpasture’s syndrome
Bullous pemphigoid
Graves’ disease
Myasthenia gravis

Front 225

Diseases caused by hypersensitivity

Hemolytic anemia

Back 225

Type II

Front 226

Diseases caused by hypersensitivity

Idiopathic thrombocytopenic purpura

Back 226

Type II

Front 227

Diseases caused by hypersensitivity

Erythroblastosis fetalis

Back 227

Type II

Front 228

Diseases caused by hypersensitivity

Rheumatic fever

Back 228

Type II

Front 229

Diseases caused by hypersensitivity

Goodpasture’s syndrome

Back 229

Type II

Front 230

Diseases caused by hypersensitivity

Bullous pemphigoid

Back 230

Type II

Front 231

Diseases caused by hypersensitivity

Graves’ disease

Back 231

Type II

Front 232

Diseases caused by hypersensitivity

Myasthenia gravis

Back 232

Type II

Front 233

Diseases caused by hypersensitivity

Type III

Back 233

Lupus
Rheumatoid arthritis
Polyarteritis nodosum
Post-streptococcal glomerulonephritis
Serum sickness
Arthus reaction
Hypersensitivity pneumonitis

Front 234

Diseases caused by hypersensitivity

Lupus

Back 234

Type III

Front 235

Diseases caused by hypersensitivity

Rheumatoid arthritis

Back 235

Type III

Front 236

Diseases caused by hypersensitivity

Polyarteritis nodosum

Back 236

Type III

Front 237

Diseases caused by hypersensitivity

Post-streptococcal glomerulonephritis

Back 237

Type III

Front 238

Diseases caused by hypersensitivity

Serum sickness

Back 238

Type III

Front 239

Diseases caused by hypersensitivity

Arthus reaction

Back 239

Type III

Front 240

Diseases caused by hypersensitivity

Hypersensitivity pneumonitis

Back 240

Type III

Front 241

Diseases caused by hypersensitivity

Type IV

Back 241

Type 1 diabetes mellitus
Multiple sclerosis
Guillain-Barré syndrome
Hashimoto’s thyroiditis
Graft-versus-host disease
PPD (test for M. tuberculosis)
Contact dermatitis

Front 242

Diseases caused by hypersensitivity

Type 1 diabetes mellitus

Back 242

Type IV

Front 243

Diseases caused by hypersensitivity

Multiple sclerosis

Back 243

Type IV

Front 244

Diseases caused by hypersensitivity

Guillain-Barré syndrome

Back 244

Type IV

Front 245

Diseases caused by hypersensitivity

Hashimoto’s thyroiditis

Back 245

Type IV

Front 246

Diseases caused by hypersensitivity

Graft-versus-host disease

Back 246

Type IV

Front 247

Diseases caused by hypersensitivity

PPD

Back 247

Type IV

Front 248

Diseases caused by hypersensitivity

Contact dermatitis

Back 248

Type IV

Front 249

↓ production of: B cells

Back 249

Bruton’s agammaglobulinemia

Front 250

↓ production of: T Cells

Back 250

Thymic aplasia (DiGeorge
syndrome)

Front 251

↓ production of: B and T cells

Back 251

severe combined immunodeficiency
(SCID)

Front 252

Bruton’s agammaglobulinemia
mech

Back 252

↓ production of: B cells

X-linked recessive defect in a tyrosine kinase gene associated with low levels of all classes of immunoglobulins.

Front 253

Bruton’s agammaglobulinemia

inheritance

Back 253

X-linked recessive

Front 254

Bruton’s agammaglobulinemia

clinical findings

Back 254

recurrent Bacterial infections after 6 months of age, when levels of maternal IgG antibody decline. Occurs in Boys

Front 255

recurrent Bacterial infections after 6 months of age, when levels of maternal IgG antibody decline. Occurs in Boys (X-linked).

Back 255

Bruton’s agammaglobulinemia

Front 256

DiGeorge syndrome aka

Back 256

Thymic aplasia

Front 257

Thymic aplasia aka

Back 257

DiGeorge syndrome

Front 258

DiGeorge syndrome
mnemonic

Back 258

CATCH-22
C = cardiac defects,
A = abnormal facies,
T = thymic hypoplasia,
C = cleft palate,
H = hypocalcemia (tetany)from parathyroid aplasia,
22 = microdeletions in chromosome 22- 22q11 deletion

Front 259

DiGeorge syndrome
mech

Back 259

↓ production of: T Cells

Thymus and parathyroids fail to develop owing to failure of development of the 3rd and 4th pharyngeal pouches.

Front 260

severe combined immunodeficiency
(SCID)

mech/causes

Back 260

Defect in early stem-cell differentiation.
↓ production of: B and T Cells

May have multiple causes (e.g., failure to synthesize MHC II antigens, defective IL-2 receptors, or adenosine deaminase deficiency).

Front 261

severe combined immunodeficiency
(SCID)

clinical findings

Back 261

recurrent viral, bacterial, fungal, and protozoal infections.

Front 262

recurrent viral, bacterial, fungal, and protozoal infections.

Back 262

severe combined immunodeficiency
(SCID)

Front 263

IL-12 receptor deficiency

mech and findings

Back 263

↓ activation of: T-cells


Presents with disseminated mycobacterial infections.

Front 264

↓ activation of: T-cells

Presents with disseminated mycobacterial infections.

Back 264

IL-12 receptor deficiency

Front 265

hyper-IgM syndrome

mech

Back 265

↓ activation of: B-cells

Defect in CD40 ligand on CD4 T helper cells leads to inability to class switch.

Front 266

↓ activation of: B-cells

Back 266

hyper- IgM syndrome

Wiskott-Aldrich
syndrome

Front 267

↓ activation of: Macrophages

Back 267

Job’s syndrome

Front 268

hyper-IgM syndrome

clinical findings

Back 268

Presents early in life with severe pyogenic infections.

Front 269

hyper-IgM syndrome

lab findings

Back 269

High levels of IgM; very low levels of IgG, IgA, and IgE.

Front 270

Wiskott-Aldrich syndrome

mech

Back 270

↓ activation of: B-cells

X-linked recessive defect in the ability to mount an IgM response to capsular polysaccharides of
bacteria.

Front 271

Wiskott-Aldrich syndrome

inheritance

Back 271

X-linked recessive

Front 272

Defect in CD40 ligand on CD4 T helper cells leads to inability to class switch.

Back 272

hyper-IgM syndrome

Front 273

defect in the ability to mount an IgM response to capsular polysaccharides of
bacteria.

Back 273

Wiskott-Aldrich syndrome

Front 274

Wiskott-Aldrich syndrome

clinical findings

Back 274

Triad of symptoms includes recurrent pyogenic Infections, thrombocytopenic
Purpura, Eczema (W-IPE).

Front 275

Wiskott-Aldrich syndrome

lab findings

Back 275

elevated IgA levels, normal IgE levels, and low IgM levels.

Front 276

Job’s syndrome

mech

Back 276

↓ activation of: Macrophages

Failure of γ-interferon production by helper T cells. Neutrophils fail to respond to
chemotactic stimuli.

Front 277

Job’s syndrome

clinical findings

Back 277

recurrent “cold” (noninflamed) staphylococcal abscesses, eczema, coarse facies, retained primary teeth,

Front 278

Job’s syndrome

lab findings

Back 278

and high levels of IgE.

Front 279

recurrent “cold” (noninflamed) staphylococcal abscesses, eczema, coarse facies, retained primary teeth,

Back 279

Job’s syndrome

Front 280

Phagocytic cell deficiency:

name them

Back 280

Leukocyte adhesion deficiency syndrome

Chédiak-Higashi
disease

Chronic granulomatous disease

Front 281

Leukocyte adhesion deficiency syndrome

mech

Back 281

Phagocytic cell deficiency

Defect in LFA-1 adhesion proteins on phagocyte

Front 282

Leukocyte adhesion deficiency syndrome

clinical findings

Back 282

early with severe pyogenic
and fungal infections and delayed separation of umbilicus.

Front 283

early with severe pyogenic
and fungal infections and delayed separation of umbilicus

Back 283

Leukocyte adhesion deficiency syndrome

Front 284

Chédiak-Higashi disease

mech

Back 284

Phagocytic cell deficiency

Defect in microtubular function and lysosomal emptying of
phagocytic cells.

Front 285

Chédiak-Higashi disease

inheritance

Back 285

AR

Front 286

Chédiak-Higashi disease

clinical presentation

Back 286

Presents with recurrent pyogenic infections by staphylococci and
streptococci, partial albinism, and peripheral neuropathy.

Front 287

Presents with recurrent pyogenic infections by staphylococci and
streptococci, partial albinism, and peripheral neuropathy

Back 287

Chédiak-Higashi disease

Front 288

Chronic granulomatous disease

mech

Back 288

Defect in phagocytosis of neutrophils owing to lack of NADPH oxidase activity or
similar enzymes.

Front 289

Defect in phagocytosis of neutrophils owing to lack of NADPH oxidase activity or
similar enzymes.

Back 289

Chronic granulomatous disease

Front 290

Chronic granulomatous disease

Clinical findings

Back 290

Presents with marked susceptibility to opportunistic infections
with bacteria, especially S. aureus, E. coli, and Aspergillus.

Front 291

Chronic granulomatous disease

Dx

Back 291

Diagnosis confirmed
with negative nitroblue tetrazolium dye reduction test.

Front 292

Presents with marked susceptibility to opportunistic infections
with bacteria, especially S. aureus, E. coli, and Aspergillus.

Back 292

Chronic granulomatous disease

Front 293

Diagnosis confirmed
with negative nitroblue tetrazolium dye reduction test.

Back 293

Chronic granulomatous disease

Front 294

Idiopathic dysfunction of: T cells

Back 294

chronic mucocutaneous candidiasis

Front 295

chronic mucocutaneous candidiasis

Mech

Back 295

Idiopathic dysfunction of: T cells

T-cell dysfunction specifically against Candida albicans

Front 296

T-cell dysfunction specifically against Candida albicans

Back 296

chronic mucocutaneous candidiasis

Front 297

chronic mucocutaneous candidiasis

clinical findings

Back 297

skin and mucous membrane Candida infections.

Front 298

Idiopathic dysfunction of: B cells

name them

Back 298

-selective immunoglobulin
deficiency
-ataxia telangiectasia
-common variable immunodeficiency

Front 299

selective immunoglobulin
deficiency

mech

Back 299

Idiopathic dysfunction of: B cells

Deficiency in a specific class of immunoglobulins––possibly due to a defect in isotype
switching.

Front 300

selective immunoglobulin
deficiency

most common

Back 300

Selective IgA deficiency is the most common

Front 301

selective immunoglobulin
deficiency

clinical findings

Back 301

sinus and lung infections; milk allergies and diarrhea are
common.

Front 302

ataxia-telangiectasia

mech

Back 302

Idiopathic dysfunction of: B cells

Defect in DNA repair enzymes with associated IgA deficiency.

Front 303

ataxia-telangiectasia

clinical findings

Back 303

Presents with cerebellar
problems (ataxia) and spider angiomas (telangiectasia).

Front 304

common variable immunodeficiency

mech and who

Back 304

Idiopathic dysfunction of: B cells

Normal numbers of circulating B cells, ↓ plasma cells, ↓ Ig, can be acquired in 20's-30's

Front 305

Autoantibodies and associated disorders

Antinuclear antibodies (ANA)

Back 305

SLE

Front 306

Autoantibodies and associated disorders

Anti-dsDNA

Back 306

Specific for SLE

Front 307

Autoantibodies and associated disorders

anti-Smith

Back 307

Specific for SLE

Front 308

Autoantibodies and associated disorders

Antihistone

Back 308

Drug-induced lupus

Front 309

Autoantibodies and associated disorders

Drug-induced lupus

Back 309

Antihistone

Front 310

Autoantibodies and associated disorders

SLE (general)

Back 310

Antinuclear antibodies (ANA)

Front 311

Autoantibodies and associated disorders

Specific for SLE

Back 311

Anti-dsDNA

anti-Smith

Front 312

Autoantibodies and associated disorders

Anti-IgG

Back 312

Rheumatoid arthritis

Front 313

Autoantibodies and associated disorders

Rheumatoid arthritis

Back 313

Anti-IgG (rheumatoid factor)

Front 314

Autoantibodies and associated disorders

Antineutrophil

Back 314

Vasculitis

Front 315

Autoantibodies and associated disorders

Vasculitis

Back 315

Antineutrophil (C-ANCA, P-ANCA)

Front 316

Autoantibodies and associated disorders

Anti-Scl-70

Back 316

Scleroderma (diffuse)

Front 317

Autoantibodies and associated disorders

Anticentromere

Back 317

Scleroderma (CREST)

Front 318

Autoantibodies and associated disorders

Scleroderma (CREST)

Back 318

Anticentromere

Front 319

Autoantibodies and associated disorders

Scleroderma (diffuse)

Back 319

Anti-Scl-70

Front 320

Autoantibodies and associated disorders

Antimitochondrial

Back 320

1° biliary cirrhosis

Front 321

Autoantibodies and associated disorders

1° biliary cirrhosis

Back 321

Antimitochondrial

Front 322

Autoantibodies and associated disorders

Antigliadin

Back 322

Celiac disease

Front 323

Autoantibodies and associated disorders

Celiac disease

Back 323

Antigliadin

Front 324

Autoantibodies and associated disorders

Anti–basement membrane

Back 324

Goodpasture’s syndrome

Front 325

Autoantibodies and associated disorders

Goodpasture’s syndrome

Back 325

Anti–basement membrane

Front 326

Autoantibodies and associated disorders

Anti–epithelial cell (desmoglein)

Back 326

Pemphigus vulgaris

Front 327

Autoantibodies and associated disorders

Pemphigus vulgaris

Back 327

Anti–epithelial cell (desmoglein)

Front 328

Autoantibodies and associated disorders

Anti-hemidesmosomes

Back 328

Bullous pemphigoid

Front 329

Autoantibodies and associated disorders

Bullous pemphigoid

Back 329

Anti-hemidesmosomes

Front 330

Autoantibodies and associated disorders

Antimicrosomal

Back 330

Hashimoto’s thyroiditis

Front 331

Autoantibodies and associated disorders

Hashimoto’s thyroiditis

Back 331

Antimicrosomal

Antithyroglobulin

Front 332

Autoantibodies and associated disorders

Antithyroglobulin

Back 332

Hashimoto’s thyroiditis

Front 333

Autoantibodies and associated disorders

Anti-Jo-1

Back 333

Polymyositis, dermatomyositis

Front 334

Autoantibodies and associated disorders

Polymyositis, dermatomyositis

Back 334

Anti-Jo-1

Front 335

Autoantibodies and associated disorders

Anti-SS-A

Back 335

aka anti Ro

Sjogren's syndrome

Front 336

Autoantibodies and associated disorders

Anti-SS-B

Back 336

aka anti La

Sjogren's syndrome

Front 337

Autoantibodies and associated disorders

Sjogren's syndrome

Back 337

Anti - SSA/Ro
Anti -SSB/La

and often ANA positive

Front 338

Autoantibodies and associated disorders

Anti-U1 RNP

Back 338

Mixed connective tissue disease

Front 339

Autoantibodies and associated disorders

Mixed connective tissue disease

Back 339

Anti-U1 RNP (Ribonucleoprotein)

Front 340

Autoantibodies and associated disorders

Anti-smooth muscle

Back 340

Autoimmune Hepatitis

Front 341

Autoantibodies and associated disorders

Autoimmune Hepatitis

Back 341

Anti-smooth muscle

Front 342

Autoantibodies and associated disorders

Anti-glutamate decarboxylase

Back 342

DM type I

Front 343

Autoantibodies and associated disorders

DM type I

Back 343

Anti-glutamate decarboxylase

Front 344

Autoantibodies and associated disorders

C-ANCA

Back 344

Wegener's granulomatosis

Front 345

Autoantibodies and associated disorders

P-ANCA

Back 345

microscopic polyangiitis

and focal necrotising and crescentic glomerulonephritis.

sometimes Churg-Strauss

Front 346

Autoantibodies and associated disorders

sometimes Churg-Strauss

Back 346

P-ANCA (anti myeloperoxidase)

Front 347

Autoantibodies and associated disorders

Wegener's granulomatosis

Back 347

C-ANCA (anti Protinase 3)

Front 348

Autoantibodies and associated disorders

focal necrotising and crescentic glomerulonephritis.

Back 348

P-ANCA (anti myeloperoxidase)

Front 349

Autoantibodies and associated disorders

microscopic polyangiitis

Back 349

P-ANCA (anti myeloperoxidase)

Front 350

Anti-neutrophil cytoplasmic antibodies aka

Back 350

ANCA

Front 351

ANCA aka

Back 351

Anti-neutrophil cytoplasmic antibodies

Front 352

perinuclear-staining antineutrophil cytoplasmic antibodies aka

Back 352

P-ANCA

Front 353

P-ANCA what letters stand for

Back 353

perinuclear-staining antineutrophil cytoplasmic antibodies

Front 354

cytoplasmic-staining antineutrophil cytoplasmic antibodies aka

Back 354

C-ANCA

Front 355

C-ANCA what letters stand for

Back 355

cytoplasmic-staining antineutrophil cytoplasmic antibodies

Front 356

HLA subtype associations

B27

Back 356

PAIR.

Psoriasis,
Ankylosing spondylitis, Inflammatory bowel disease, Reiter’s syndrome.

Front 357

HLA subtype associations

Psoriasis

Back 357

B27

Front 358

HLA subtype associations

Ankylosing spondylitis

Back 358

B27

Front 359

HLA subtype associations

Inflammatory
bowel disease

Back 359

B27

Front 360

HLA subtype associations

Reiter’s syndrome.

Back 360

B27

Front 361

HLA subtype associations

B8

Back 361

Graves’ disease, celiac sprue.

Front 362

HLA subtype associations

celiac sprue.

Back 362

B8

Front 363

HLA subtype associations

Graves’ disease

Back 363

B8

Front 364

HLA subtype associations

DR2

Back 364

Multiple sclerosis, hay fever, SLE, Goodpasture’s.

Front 365

HLA subtype associations

Multiple sclerosis

Back 365

DR2

Front 366

HLA subtype associations

hay fever

Back 366

DR2

Front 367

HLA subtype associations

SLE

Back 367

DR2

Front 368

HLA subtype associations

Goodpasture’s.

Back 368

DR2

Front 369

HLA subtype associations

DR3

Back 369

Diabetes mellitus type 1.

Front 370

HLA subtype associations

Diabetes mellitus type 1.

Back 370

DR3 and DR4

Front 371

HLA subtype associations

DR4

Back 371

Rheumatoid arthritis, diabetes mellitus type 1.

Front 372

HLA subtype associations

Rheumatoid arthritis

Back 372

DR4

Front 373

HLA subtype associations

diabetes mellitus type 1.

Back 373

DR3 and DR4

Front 374

HLA subtype associations

Pernicious anemia

Back 374

DR5

Front 375

HLA subtype associations

Hashimoto’s thyroiditis.

Back 375

DR5

Front 376

HLA subtype associations

Steroid-responsive nephrotic syndrome.

Back 376

DR7

Front 377

HLA subtype associations

DR7

Back 377

Steroid-responsive nephrotic syndrome.

Front 378

Hyperacute rejection

description, time, and mechanism

Back 378

Antibody mediated due to the presence of preformed antidonor antibodies in the
transplant recipient. Occurs within minutes after transplantation.

Front 379

Acute rejection

description, time, and mechanism

Back 379

Cell mediated due to cytotoxic T lymphocytes reacting against foreign MHCs. Occurs
weeks after transplantation.

Front 380

Acute rejection

Tx

Back 380

Reversible with immunosuppressants such as cyclosporin and OKT3.

Front 381

Chronic rejection

description, time, and mechanism

Back 381

Antibody-mediated vascular damage (fibrinoid necrosis); occurs months to years after
transplantation. Irreversible.

Front 382

Graft-versus-host disease

description, time, and mechanism

Back 382

Grafted immunocompetent T cells proliferate in the irradiated immunocompromised
host and reject cells with “foreign” proteins, resulting in severe organ dysfunction.

Front 383

Graft-versus-host disease

findings

Back 383

Major symptoms include a maculopapular rash, jaundice, hepatosplenomegaly, and
diarrhea.