Imm-Fa

Front 1

lymph drainage in body

Back 1

rt lymphatic duct drains rt arm and rt half of head

thoracic duct drains everything else

Front 2

follicle
-where in LN is it?
-desc

Back 2

-in cortex of LN
(LN cortex contains follicle (B cells) & paracortex (T cells))

-site of B cell proliferation
-in outer cortex, primary follicles are dormant & dense
-secondary follicles are active & pale in their germinal centers

Front 3

medulla

Back 3

consists of:

*medullary cords=closely packed lymphocytes and plasma clels

*medullary sinuses
-communicate with efferent lymphatics
-contain reticular cells and macrophages

Front 4

paracortex

-when is it enlarged?
-when is it small?

Back 4

-houses T cells
-region of cortex b/w cortex and medulla
-conains high endothelial venules thru which T and B cells enter blood
==>thus paracortex becomes very enlarged during extreme cellular immmune response

-not well developed in DiGeorge syndrome

Front 5

sinusoids of spleen
-desc
-where in spleen?

-where find T cells
-where find B cells

Back 5

-long vascular channels within red pulp of spleen
-fenestrated "barrel hoop" BM
-macrophages nearby

T cells in:
*PALS (Periarterial lymphatic sheath)
*red pulp

B cells in follicles (white pulp)

Front 6

thymus
-T cells derive from what embryonic tissue?
-cortex contains ?
-medulla contains ?

-what is positive and negative selection?
-where do positive and negative selection occur?

Back 6

-site of T cell differentiation and maturation
-encapsulated

-arises from 3rd brachial pouch
-lymphocytes (T) are of mesenchymal origin

-cortex is dense w/immature T cells

-medulla is pale & contains:
*mature T cells
*epithelial reticular cells
*Hassall's corpuscles

-positive selection (MHC restriction) & negative selection (non-reactive to self) occur @ corticomedullary jxn

Front 7

Th1 cells produce

Back 7

IL2
IFN-gamma
activate macs & cytotoxic T cells

Front 8

Th2 cells producd

Back 8

IL-2
IL-4
IL-5
help B cells make Ig (IgE>IgG)

Front 9

innate immunity:
what actors are involved?

Back 9

neutrophils
macs
dendritic cells
complement

Front 10

adaptive immunity:
what actors are involved?

Back 10

T cells
B cells
circulating Ig

Front 11

MHC encoded by what genes?

Back 11

MHC (Major Histocompatibility Complex) coded by HLA (Human Leukocyte Antigen) genes

Front 12

MHC I vs. MHC II
-why important
-encoded by what genes
-expressed on what cells
-where is Ag loaded

Back 12

MHC I:
*mediates viral immunity

-encoded by HLA-A, B, and C
-pairs with B2 microglobulin
-expressed on all nucleated cells
-Ag is loaded in RER of mostly intracellular peptides


MHC II:
*main determinants of organ rejection
-encoded by HLA-DP, DQ, DR
-expressed only on APC's
-Ag loaded in an acidified endosome

Front 13

what are the main determinants of organ rejection

Back 13

MHC II's

Front 14

APC cells--ex's

Back 14

Macs
B cells
Dendritic cells

Front 15

what do Cytotoxic T cells bind?

Back 15

Cytotoxic T cells have CD8, which bind MHCI mcs on virus-infected cells

Front 16

cell w/CD8+ is called what?
cell w/CD4+ is called what?

Back 16

cytotoxic T cell=cell w/CD8+
helper T cell=cell w/CD4+

Front 17

what CD's do B cells have?

Back 17

CD 19, 20

Front 18

CD3 complex

Back 18

cluster of polypeptides assoc w/TCR

imp in signal transduction

Front 19

Ig:
Fab vs. Fc segment

Back 19

Fab=
"a"ntigen "b"inding segment
-composed of heavy and light chains

Fc=
(composed only of heavy chains)
"c"omplement-binding region (IgG+IgM only)
"c"onstant
"c"arboxy terminal
"c"arbohydrate side chains

Front 20

opsonization

Back 20

=phagocytosis of bacteria

(Ig covers the pathogen==>promotes phagocytosis)

Front 21

neutralization

Back 21

Ig covers the pathogen==>prevents bacterial adherence to cell

Front 22

Ig's role in complement

Back 22

Ig covers the bacteria==>more likely to activate complement
==>enhances opsonization (phagocytosis) of bacteria and lysis

Front 23

what generates antibody diversity

Back 23

1. random recombination of VDJ (heavy chain) or VJ (light chain) segments

2. combination of light and heavy chains

3. somatic hypermutation

4. add'n of nucleotides to DNA during "genetic recombination" by terminal deoxynucleotidyl transferase

Front 24

Ig isotypes: most common to least common

Back 24

G > A > M > D > E

Front 25

what Ig's do most mature B cells express?

Back 25

Ig M and D

They can switch to G, A, or E via isotype switching

Front 26

IgG fxns

Back 26

-MC Ig (G>A>M>D>E)

*fix complement
*cross placenta
*secondary antibody response
*opsonizes bacteria
*neutralizes bacterial toxins and viruses (coats their surface so they cannot adhere to tissue)

Front 27

IgM fxns

Back 27

-primary response to Ag
-fix complement but does not cross placenta
-all mature B cells express IgM (and IgD) but can switch to Ig G, A, or E via isotype switching
-monomer or pentamer (huge!)

Front 28

IgA fxns

Back 28

"secretory Ig": picks up secretory component from epithelial cells before secretion
-found in secretions (ie breast milk)
-prevents bacterial and viral adherence to mucosal surfaces
-does not fix complement (only IgM and IgG fix complement)

Front 29

Goljan: most potent activator of complement system

Back 29

IgM

Front 30

IgE fxns

Back 30

-Type 1 hypersensitivity:
IgE exposed to Ag
==>IgE induces release of mediators from mast cells and B cells

*mediates immunity to worms

-lowest concentration of the Ig's

Front 31

which Ig mediates immunity to worms

Back 31

Ig E

Front 32

isotype
-desc
-what determines it

Back 32

isotype=IgG, IgA, IgM, IgD, or IgE

Ig epitope common to a single class of Ig (determined by heavy chain)

Front 33

what determines whether an Ig is IgG, IgA, IgM, etc

Back 33

the heavy chain

Front 34

allotype of Ig

Back 34

=polymorphism

Ig epitope that differs b/w different members of same species
("allo"=different members of same species, eg allograft)

Front 35

idiotype of Ig

Back 35

-specific for a given Ag

-Ig epitope determined by Ag-binding site

Front 36

helper T cells-

cell surface proteins

Back 36

TCR
CD3
CD4
CD28
CD40L

Front 37

cytotoxic T cells-

cell surface proteins

Back 37

TCR
CD3
CD8

Front 38

B cells-

cell surface proteins

Back 38

IgM
B7
MHCII

CD19
CD20
CD40

Front 39

Macrophages-

cell surface proteins

Back 39

MHCII
CD14
Receptors for Fc
Receptors for C3b

Front 40

NK cells-

cell surface proteins

Back 40

receptors for MHCI

CD16
CD56

Front 41

all cells except mature RBC's have what cell surface protein?

Back 41

MHCI

Front 42

what stimulates dendritic cells to migrate to lymph nodes?

Back 42

TNF-alpha

Front 43

TNF-alpha
-secreted by what
-fxns

Back 43

-secreted by macs

*B cell proliferation
*IL-2 receptor synthesis by Th cells
*attracts & + neutrophils
*stimulates dendritic cell to migrate to LN

Front 44

IL-6
-secreted by what
-fxns

Back 44

-secreted by Th & macs

*production of acute phase reactants
*production of Ig

Front 45

IL-8
-secreted by what
-fxns

Back 45

-secreted by Th

*neutrophil chemotactic factor

Front 46

IFN-gamma
-secreted by what
-fxns

Back 46

-secreted by Th
-stimulates macs

Front 47

interferons
-desc
-MOA

fxns of:
-alpha-IFN
-beta-IFN
-gamma-IFN

Back 47

=interfons "interfere" w/viral synthesis
-induce production of 2nd protein that inhibits viral protein synthesis by degrading viral mRNA (but not host mRNA)

-place uninfercted cells in anti-viral state

-alpha-IFN & beta-IFN (-) viral protein syntehesis

-gamma-IFN (IFN-gamma) incr MHC I & II expression and antigen presentation in all cells

-activates NK cells to kill virus-infected cells

Front 48

active vs. passive immunity

Back 48

active immunity--you contracted the dz yourself and mkae your own Ig (takes awhile but then you have memory cells for life)

passive immunity-you are given Ig from another person to Tx dz they were just exposed to; rapid onset but fast offset
*Ig administered (passive) for ppl exposed to Tetanus, Botulinum, HepB, and Rabies:
*mneum: "To Be Healed Rapidly"

Front 49

which pathogen has 2 flagellar variants?

Back 49

Salmonella (think of a salmon with its 2 flagella flapping as it swins)

Front 50

relapsing fever

Back 50

Borrelia

Front 51

which pathogen has programmed antigenic rearrangement?

Back 51

trypanosomes (parasisite)

Front 52

which bacteria uses a pilus protein?

Back 52

Neisseria

Front 53

anergy

Back 53

-self-reactive T cells (bad!) become non-reactive without co-stimulatory mcs

-B cells also become anergic, but tolerance is less complete than in T cells

Front 54

Arthus Rxn

Back 54

type of Type III hypersens.

(serum sickness (ImCo) is more common than Arthus Rxn)

Arthus Rxn=
-inject Ag into skin
-Ig bind Ag
-Ag-Ig complexes deposit in skin
==>activate complement
==>edema, necrosis

Front 55

Type IV hypersensitivity

Back 55

=Delayed T cell mediated hypersens.

mneum: "4 T's"
-T cells (Th1)
-TB skin tests
-Touching (i.e. poison ivy)
-Transplant rejxn

Front 56

hemolytic anemia is mediated by which type of hypersensitivity

Back 56

Type II (Ig against RBC)

Front 57

MG is mediated by which type of hypersensitivity

Back 57

Type II (Ig against Ach-R)

Front 58

erythroblastosis fetalis is mediated by which type of hypersensitivity

Back 58

Type II (Ig against Rh+ in baby)

Front 59

Rheumatic fever is mediated by which type of hypersensitivity

Back 59

Type II (Ig against receptor)

Front 60

the pathogenesis of which derm problem involves hypersensitivity

Back 60

bullous pemphigoid=Type II hypersen

Front 61

Rh arthritis is mediated by which type of hypersensitivity

Back 61

Type III (ImCo)

There is IgM that is Anti-IgG
==>IgM-IgG complexes settle on joints

Front 62

polyarteritis nodosum is mediated by which type of hypersensitivity

Back 62

type III

(P-ANCA)

Front 63

post-strep glomerulonephritis is mediated by which type of hypersensitivity

Back 63

type III

Front 64

Arthus rxn is mediated by which type of hypersensitivity

Back 64

Type III

Front 65

hypersensitivity pneumonitis is mediated by which type of hypersensitivity

Back 65

type III

Front 66

Type I DM is mediated by which type of hypersensitivity

Back 66

Type IV

Front 67

MS is mediated by which type of hypersensitivity

Back 67

Type IV

Front 68

Guillain Barre is mediated by which type of hypersensitivity

Back 68

Type IV

Front 69

GVHD is mediated by which type of hypersensitivity

Back 69

Type IV

Front 70

Hashimoto's thyroiditis is mediated by which type of hypersensitivity

Back 70

Type IV (First aid p. 194)

Front 71

contact dermatitis is mediated by which type of hypersensitivity

Back 71

Type IV

Front 72

what chronic dz's are mediated by Type IV hypersensitivity

Back 72

Type I DM
Hashimoto's thyroiditis
MS
Guillain-Barre

Front 73

DiGeorge Syndrome
-desc
-genetics (deletion)

Back 73

"T"hymic & para"T"hyroid aplasia (b/c aplasia of 3rd & 4th pharyngeal pouches)
==>deficient "T" cells
==>recurrent viral and fungal infxns

-"T"etany d/t hypocalcemia
-congenital defect of heart and great vessels
*22q11 deletion

Front 74

22q11 deletion is assoc with what dz

Back 74

DiGeorge

Front 75

Bruton's agammaglobulinemia
-desc
-pg

Back 75

"B"'s:

"B"rutons=
deficient "B" cells=
"B"acterial infxns
"B"oys (X-linked)

-X-linked recessive defect in V(H) (heavy chain) gene segments to undergo gene arrangment
==>defective tyrosine kinase gene which is required for maturation of pre-B cells to mature B cells
==>arrest B cell development in pre-B cell stage
==>low levels of all Ig

Front 76

SCID
-desc
-et

Back 76

SCID=Severe Combined Immunodeficiency Dz

-deficient B and T cells==>recurrent:

Bacterial
Viral
Fungal
Protozoal

infxns

many possible causes:
-ADA deficiency ("SCID ADA TL"; ADA=Adenosine Deaminase)
-defective IL-2 receptors
-failure to synthesize MHCII

Front 77

IL-12 deficiency:

how present

Back 77

present w/multiple mycobacterial infxns

IL-12 activates Th1 cells & NK cells and Th1 cells;

Th1 cells are required to kill Mycobacteria, i.e. in Mycobacteria tuberculosis:

-MƏ (APC’s with MHC II) present Ag to CD4+ Th cells

-MƏ release:
*IL-1→activates Th1, fever
*IL-12→(+) Th1 formation

Th1 cells release:
*IL-2
→(+) Th1 proliferation (positive feedback)
→Activates monocytes→MƏ

*IFN-γ→(+) MƏ to kill tb

Lipids from killed tubercle bacillus→caseous nec
Activated MƏ fuse→multinucleated giant cells

Front 78

hyper-IgM syndrome
-et
-desc
-presentation

Back 78

-caused by defect in CD40L ligand on Th cells
==>cannot class switch (interaxn b/w CD40L on Th cells & CD40 on B cells is req for isotype switching)
==>high levels of IgM, low levels of IgA, IgG, IgE

-present w/severe pyogenic URT and LRT infxns early in life (pyogenic infxn= bacteria that produces pus/abscesses, i.e. SA)

Front 79

Wiskott-Aldrich syndrome
-inheritance pattern
-desc
-serum levels
-Sx

Back 79

-X-linked (wiSKOTT (~Scott)=boy=X-linked)

*Imagine a boy named SKOTT with these Sx (recurrent infxns & bleeds to death)

(some info from HY CB p. 154)

1. Thrombocytopenia
==>purpura
==>bleeding = MCCoD
(prolonged bleeding at umbilical stump or after circumcision)

2. inab to mount IgM response against capsular polysaccharide of bacteria:

H flu
Strep
N men

(these bugs have polysacchide capsules; thus these are the same bugs that infect ppl with sickle cell anemia & asplenic pts)


[mneum: "WIPE" ("IPE"=triad of Sx)

W=Wiscott Aldrich
I=recurrent pyogenic Infxns
P=thrombocytic Purpura
E=Eczema]

Front 80

Job's syndrome
-pathogenesis
-presentation

Back 80

Th1 cells fail to produce IFN-gamma
==>no activation of macs
==>neutrophils fail to respond to chemotactic stimuli

Presentation:
-"cold" (noninflamed) Staph aureus infxns
-eczema
-coarse facies
-high IgE levels
-retained primary teeth

Front 81

leukocyte adhesion
-pathogenesis
-presentation

Back 81

-defect in LFA-1 adhesion proteins on phagocytes
-presents with:
*pyogenic and fungal infxns
*delayed separation of umbilicus

Front 82

Chediak-Higashi syndrome

Back 82

AR;

defect in microtubular functioning and lysosomal emptying of phagocytic cells

Presentation:
-recurrent Staph and Strep infxns
-partial albinism
-peripheral neuropathy

Front 83

chronic granulomatous dz
-desc
-inheritance pattern

Back 83

[RR Path p. 16]

-X-rec

lack NADPH oxidase
==>reduced production of superoxide radical
==>no respiratory burst (resp burst requires superoxide radical & H2O2)
==>neutrophils cannot phagocytose things

Present:
lots of infxns, esp
-Staph
-E coli
-Aspergillus

Dx confirmed w/negative nitroblue tetrazolium dye reduction test (test is negative b/c no respiratory burst (resp burst requires superoxide radical & H2O2))

Front 84

chronic mucocutaneous Candidiasis
-et

Back 84

T-cell dysfxn specifically regarding Candida
==>skin and mucous membrane candidiasis

Front 85

selective IgA deficiency
-desc
-et

Back 85

==>problems w/secretions and mucous membranes (that's what "secretory IgA" affects)
*sinus and lung infxns
*milk allergies, diarrhea


-d/t problems w/class switching (can't switch from IgM==>IgA)

Front 86

ataxia-telangiectasias

-inheritance pattern
-et
-Sx
-assoc w ?

Back 86

-AR

defect in DNA repair enzymes
==>cerebellar prob (ataxia)
==>spider angiomas (telangiectasias)

*associated IgA deficiency

Front 87

common variable immunodeficiency

Back 87

-nl # circulating B cells, but...

decr #plasma cells==>decr Ig

Front 88

ANA

Back 88

SLE

Front 89

anti-ds DNA

Back 89

specific for SLE

Front 90

anti-Smith

Back 90

specific for SLE

Front 91

anti-histone Ig

Back 91

drug-induced SLE

Front 92

anti-IgG Ig

Back 92

=Rh factor

Rh arthritis

Front 93

anti-neutrophil Ig
-ex
-suggests what

Back 93

eg. C-ANCA, P-ANCA

-suggests vasculitis

Front 94

C-ANCA

Back 94

vasculitis

(Wegener's granulomatosis)

Front 95

P-ANCA

Back 95

vasculitis

Front 96

anti-centromere Ig

Back 96

Scleroderma (CREST) [not diffuse]

Front 97

anti-Scl-70

Back 97

scleroderma (diffuse) [not CREST]

Front 98

anti-mitochondrial Ig

Back 98

primary biliary cirrhosis

Front 99

anti-microsomal Ig

Back 99

Hashimoto's thyroiditis

Front 100

antigliadin Ig

Back 100

celiac dz (=celiac sprue)

Front 101

anti-basement membrane Ig

Back 101

Goodpasteur's

Front 102

anti-epithelial cell Ig

Back 102

pemphigus vulgaris

Front 103

anti-Jo-1 Ig

Back 103

polymyositis (=progressive symmetric proximal mm wkness d/t CD8+ destruction of myofibers)

dermatomyositis (~polymyositis but shawl-face skin rash and incr risk of malignancy)

Front 104

which dz's assoc w/

HLA B27

Back 104

"PAIR"

Psoriasis
Ankylosis spondyliasis
IBD
Reiter's syndrome

Notice how "AIR" were all in that one MSK lecture we had

Front 105

which dz's assoc w/

HLA B8

Back 105

Grave's dz
celiac sprue

Front 106

which dz's assoc w/ DR2

Back 106

Note: these are all types of hypersensitivity:

Hay fever (Type I)
Goodpasteur's (Type II)
SLE (Type III)
MS (Type IV)

Front 107

which dz's assoc w/DR3?

Back 107

Type I DM (assoc w/DR 3 & 4)

Front 108

which dz's assoc w/DR4

Back 108

Type I DM (assoc w/DR 3 & 4)
RA

Front 109

which dz's assoc w/DR5

Back 109

pernicious anemia==>B12 def
Hashimoto's thyroiditis

Front 110

which dz's assoc w/DR7

Back 110

steroid-responsive nephrotic syndrome

Front 111

hyperacute rejection
-time frame
-desc

Back 111

-within minutes
-preformed anti-donor Ig

Front 112

acute rejection
-time frame
-desc
-reversible?

Back 112

-within weeks
-Type 4 (delayed) hypersensitivity: Tc cells react against foreign MHCs

*REVERSIBLE w/immunosuppressants like cyclosporine and OKT3

Front 113

chronic rejection
-time frame
-desc
-reversible?

Back 113

-months-years
-antibody-mediated vascular damage (damage to bv)
-irreversible

Front 114

GVHD

Back 114

-immunocompetent graft reacts against immunosuppressed host
==>severe organ dysfxn==>
*macropapular rash
*jaundice
*hepatosplenomegaly
*severe diarrhea

Front 115

"cytotoxic hypersensitivity"

Back 115

Type 2 hypersensitivity

Front 116

some ex's of encapsulated bacteria (contain capsule)

-what is purpose of capsule
-how test for an encapsulated bacteria

Back 116

note: all of these cause pneumonica/meningitis:

Step pneumo
H flu
Klebsiella pneumoniae
N men

*polysaccharide capsule protects against phagocytosis

*test for encapsulated bact w/Quellung rxn: when reactant added, capsule swells ("sweLLUNG" with "QueLLUNG")

Front 117

what is an antiphagocytic virulence factor?

Back 117

polysaccharide capsule

Front 118

dipicolinic acid

Back 118

dipicolinic acid==>thus spore-forming bacteria, eg:

Bacillus cereus/anthracis
Clostridia (botulinum/tetani/diff/perf)

Front 119

Staph aureus
-virulence factor
-desc

Back 119

-virulence factor=Protein A,
which binds Fc-IgG==>prevents complement activation

causes:
1. inflammatory dz
*skin infxn
*organ abscesses
*pneumonia

2. toxin-mediated:
*TSST-1=superantigen (superantigens bind MHCII-TCR
==>polyclonal T-cell activation)
*exfoliative toxin==>scalded skin syndrome (mneum: usu exfoliation is good for your skin, but it's way too much in SA)
*entertoxin==>GI prob via preformed toxins

Front 120

rheumatic fever

Back 120

-sequelae of GAS pharyngitis (not GAS impetigo)

"rheumatic" fever gives you:
-arthritis (just like "rheumatoid" arthritis--remember Jerry in MSK lab)
-heart problem

mneum: no "rheum" for SPECCulation:

S=Subcutaneous nodules
P=Polyarthritis
E=Erythema marginatum
C=Carditis
C=Chorea

Front 121

Strep pyogenes

Back 121

=GAS

1. Pyogenic:
*pharyngitis
*cellulitis
*impetigo

2. Toxigenic
*scarlet fever
*TSS

-Ig to M protein enhances host defenses against GAS
-ASO titer detects recent GAS infxn

*Sequelae are immunologic:
mneum: "PH"aryngitis gives you glomerulonePHritis and rheumatic PHever

pharyngitis/impetigo==>glomerulonephritis

pharyngitis only==>rheumatic fever

-sequelae of GAS pharyngitis (not GAS impetigo)

"rheumatic" fever gives you:
-arthritis (just like "rheumatoid" arthritis--remember Jerry in MSK lab)
-heart problem

mneum: no "rheum" for SPECCulation:

S=Subcutaneous nodules
P=Polyarthritis
E=Erythema marginatum
C=Carditis
C=Chorea

Front 122

scarlet fever--what bug

Back 122

GAS

Front 123

TSS--what bug

Back 123

SA or GAS

Front 124

M protein

Back 124

GAS

Ig to M protein enhances host defense ag GAS

Front 125

ASO titer

Back 125

detects recent GAS infxn

Front 126

MCC meningitis

Back 126

Strep pneumo

Front 127

MCC otitis media in kids

Back 127

Strep pneumo

Front 128

MCC pneumonica

Back 128

Strep pneumo

Front 129

MCC sinusitis

Back 129

Strep pneumo

Front 130

Strep pneumo

Back 130

MCC of "MOPS":

Meningitis
Otitis media in kids
Pneumonia
Sinusitis
*encapsulated
*IgA protease

*"rusty" sputum
*sepsis in sickle cell anemia
*splenectomy

Front 131

what bug causes "rusty" sputum

Back 131

Strep pneumo

Front 132

what bact causes sepsis in sickle cell anemia

Back 132

Strep pneumo

Front 133

what bact assoc w/splenectomy

Back 133

Strep pneumo

Front 134

IgA protease

Back 134

Strep pneumo or

Front 135

Enterococcus faecalis

Back 135

=enterococci (enterococci=
Enterococcus faecalis or
Enterococcus faecium)

[enterococcus=intestine
faecalis=feces]

-cause UTI and subacute endocarditis
-grow in 6.5% NacCl
-Lancefield Group D (Enterococci and nonenterococcoal Group D strep)
-Pen-G resistant

Front 136

enterococci
-refers to what bact`

Back 136

Enterococcus faecalis or
Enterococcus faecium

[enterococcus=intestine
faecalis=feces]

-cause UTI and subacute endocarditis
-grow in 6.5% NacCl
-Lancefield Group D (Enterococci and nonenterococcoal Group D strep)
-Pen-G resistant

Front 137

Lancefield group D

Back 137

=enterococci (Enterococcus faecalis or
Enterococcus faecium)

or nonenterococcal Group D strep

Front 138

prosthetic devices and catheters

Back 138

Staph epidermidis

Front 139

Strep viridians

Back 139

-part of nl oral flora
-cause dental caries and subacute endocarditis