Bcd Micro Test 2

Front 1

important invasive factor

Back 1

IgA protease

Front 2

agglutinins and typical Ig

Back 2

clump bacteria, enhance their removal- usually IgM

Front 3

opsonins and typical Ig

Back 3

enhance phagocytosis,
Ab coated microbes attach to Fc receptor on phagocytic cells (M/M, neuts) --- IgG most often

also- complement helps

Front 4

Abs that activate complement

Back 4

IgM and IgG

Front 5

neutralizing Abs do what and typical Ig

Back 5

AB THAT NEUTRALIZE VIRUSES OR BIOLOGIC ACTIVITY OF BACTERIAL TOXINS

IgG, IgA

Front 6

lysins and typical ig

Back 6

CAUSE DISRUPTION OF CELL MEMBRANES ESPECIALLY IN CONJUCTION WITH THE C SYSTEM (IgG, IgM)

Front 7

anti-adherence Ig and example

Back 7

PREVENT ATTACHMENT OF MICROBES TO CELLS OR HARD SURFACES. FOR EX. SIgA IN SALIVA PREVENTS BACTERIA FROM ADHERING TO SURFACES OF TEETH

Front 8

what is ADCC?

Back 8

antibody-dependent cell-mediated cytotoxicity

- NK binds to Fc portion of antibody bound to pathogen and NK will release contents onto infect cells
- primary way NK cells kill

Front 9

active defense mechanisms at mucosal surfaces

Back 9

mammary gland, gastrointestinal, respiratory, urogenital

- skin isn't active

Front 10

components of GI immunology (physical// chemical/ biological barrier)

Back 10

mucous- binds lectins on pathogen surface (contains defensins that poke holes)
cilliary actions
pH
enzymes/ antimicrobial peptides (lysozyme)
leukocytes at the ready incase physical barrier is bypassed

Front 11

components of GI immunology (secondary)

Back 11

GALT
- epithelial
- lamina propria
- mesenteric lymph nodes

Front 12

oral lymphoid tissues

Back 12

- waldeyer's ring
- adenoids
- palatine tonisils
- lingual tonsits
- produce secretory IgA

Front 13

components of intestinal mucosal tissues

Back 13

- effector cells populate healthy intestinal epithelium and lamina propria
- peyer's patches (effector cells not yet active)
- lymphoid follicles
- draining lymphatics from villi to mesenteric lymph nodes
- LP has mature, active B and T cells (75% in gut- main area

Front 14

M cells
reside:
take up antigen by:
Ag transported by:
antigen then bound by:

Back 14

- in columnar epithelial along with enterocytes
- endocytosis/phagocytosis
- taken in vesicles and released at basal surface
- bound by dendritic cells, present to T cells
- lead into peyer's patches (act like regular LN)

Front 15

cell that can extend into gut lumen to capture antigen
- rest of its body sits in:

Back 15

activated lamina propria dendritic cells

sits in peyer's patch so it can be ready to present

Front 16

active effector cells in gut is constantly making _____ to protect system

Back 16

IgA

Front 17

effector cytotoxic lymphocytes that can integrate into the intestinal epithelia
- whatever it binds, it kills

can be alpha:beta or gamma:delta

Back 17

intestinal epithelial lymphocytes

Front 18

special things about mucosal immune system

- effector cells migrate:
- macrophages don't contain ______ and don't generate ___________
- function to _______ not _____ microorganisms

Back 18

effector cells always migrate back to mucosa
macs don't contain TLRs --> no inflammation
restrain, not remove (we like commensal bacteria)

Front 19

naive B and T cells that migrate through teh GALT (are/are not) specific for GALT

Back 19

not specific until activated to become GALT specific

Front 20

gut-homing effector T cells bind to ___________ to enter lamina propria

in lamina propria, they bind to _______ expressed by __________ making it __________

Back 20

- bind to intestinal vascular endothelium

- bind to chemokines (CCL225) expressed by intestinal epithelium

- embed in epithelia

Front 21

factor that allows gut-homing into lamina propria

factor for embedding into epithelia

Back 21

L-selectin & alpha4: beta7 to MAdCAM-1 on endothelium

E-cadherin on epithelium

Front 22

Abs passed to baby through breast milk

Back 22

IgA- activated in gut, is specific for all mucosa, can circulate to mammary glands then give baby Gut-specific immunity

Front 23

roles for secreted IgA

Back 23

- can export toxins from LP when secreted
- bind and neutralize Ags internalized in endosomes
- stick in mucous, can bind to toxins, bacteria, neutralizing pathogens until it gets clipped/passes through
- can bind pathogen on M cell and take it to lymphoid tissue
- picks up Ag in endosome of M cell then take to LN tissue

Front 24

why do we have two forms of IgA?

Back 24

IgA1 has longer hinge region- often cleaved by proteases
IgA2 evolved with shorter hinge- present in areas with higher amounts of cleaving pathogens

IgA1 more in oral/GI/respiratory mucosa, tonsils, spleen, saliva

Front 25

NOD receptors act like ________ to sense _______ in the intestinal epithelium

activated in response to ________, leads to ___________

Back 25

act like TLRs to sense toxins

NFkB, leads to inflammation (cytokines + defensins)

Front 26

why are gamma:delta cells places at the gut epithelial tissue?

forces ____ expression on infected cell
leads to:

Back 26

- MHC independent, don't want to wait for MHC recognition to start fighting
- forces MIC expression
- apoptosis
- gamma delta cell helps repair wound

Front 27

what happens when a cell loses its MHC I receptor?

Back 27

means its been infected

express MIC (NK receptor)

induce NK killing

Front 28

mucosal immunity against worms needs this kind of helper T cell

Back 28

TH2

- don't want to activate complement or macrophages like in TH1
- want B cell activation --> IgE production

Front 29

once immunized, over time IgM concentration and affinity:

over time IgG concentration and affinity

Back 29

stay low

increases, better affinity through somatic hypermutation

Front 30

will secondary responses produce IgM?

Back 30

- no

Front 31

how are naiive B cells inhibited from responding in a secondary response?

why is this important?

Back 31

- B cells express FcyRIIB1
- specific IgG binds to these receptors on naiive B cells and inhibit them

1. provide feedback inhibition of an ongoing immune response
2. provide competitive mechanism to drive affinity maturation

Front 32

RhoGAM prevents against this disease

disease caused by:

Back 32

newborn hemolytic anemia

1) Rh- mom reacts to Rh+ from baby, makes IgM (too big to cross barrier to baby), normal baby
2) secondary Rh+ pregnancy, would have high-affinity IgG response to baby, destroy fetal RBCS

Front 33

how does RhoGAM work

Back 33

1) given during first Rh+ pregnancy
2) is anti- Rh+ IgG
3) since all of moms cells are naiive, it will bind to all of them and inhibit them leading to no response at all

Front 34

disadvantage to inhibition of naiive B cells in specific response

Back 34

pathogens evolve over time, slow changing of Ags on surface
less and less memory as Ags are mutated and specific Abs can't recognize them, all the while inhibiting naiive cells
eventually no Ags will be recognized by memory cells and you have to start all over at a primary response

Front 35

how do we recognize memory T cells?

Back 35

surface markers differ due to mRNA splicing

CD45RA on naiive
CD45RO on memory/effector cells

Front 36

different fates of naiive T cells

Back 36

straight to memory
- central memory (stay in lymphoid tissue)
- effector memory (migrate to tissues)

straight to effector cell
- then become quiescent memory cell
- most effectors die after a few days

Front 37

3 types of failures of the body's defenses

Back 37

1. evasion/ subversion of our defense system by pathogens
2. inherited deficiencies
3. acquired deficiencies

Front 38

ways pathogens evade the immune response

Back 38

1. antigenic variation (different serotypes of the same bacteria)
2. antigenic shift (dramatic)
3. latency (herpes)

Front 39

difference between antigenic drift and shift

Back 39

drift: generation of new viral strains- relatively mild disease epidemics

shift: something we've never seen before. no immunity to a new novel hemagglutinin

Front 40

primary immunodeficiency disease characterized by lack of Abs

what symptom does it cause (especially by what kind of bacteria?)

caused by loss of this in B cells

treatment?

Back 40

bruton's agammaglobulonemia

recurrent upper respiratory infections- PYOGENIC, polio

loss of btk (bruton's tyrosine kinase) --> no B cell development without it

Ig given by IV

Front 41

most common immunodeficiency

what takes its place in the saliva?

Back 41

selective IgA deficiency

IgM

Front 42

What is DiGeorge's syndrome?

developmental or genetic?

how are B cells affected?

Back 42

lack of thymus, T cell defect

developmental (due to gene deletion- not hereditary)

lower levels because you can't make TH2 T Cells
- can only have T-independent responses of IgM

Front 43

characteristics of severe combined immunodeficiency disease (SCID)

how do you treat?

Back 43

no T or B cells

life-threatening- bone marrow transplant only treatment

Front 44

3 gene defects related to SCID

Back 44

1) IL-2 Receptor gamma chain defect (component of cytokine receptors)
2) RAG 1 or 2
3) adenosine deaminase (leads to build up of metabolic products that kill T and B cells)

Front 45

defect in chronic granulamoatous disease

what cannot be formed

Back 45

phagocytic cells can take up microbe but are unable to break them down

- can't form O2 radicals and hydrogen peroxide

Front 46

2 types of leukocyte adhesion deficiencies

both inhibit:
cause widespread:
severe ______ disease:

Back 46

LAD type I: lack of LFA-1 (integrin) on neutrophils (CD18?)

LAD type II: lack of selectin LIGAND on neutrophils

inhibit diapedesis
widespread pyogenic bacterial infections
periodontal disease

Front 47

loss of classical complement components leads to:

loss of MBL or alternative complement components leads to:

loss of MAC complement components leads to:

Back 47

immune complex diseases (often autoimmune such as lupus)

pyogenic bacterial infections or neisseria

neisseria infections (gonorrhea, meningitis)

Front 48

causes hereditary angioedema (HANE)

what does missing component normally do?

can be increased by:
symptom of concern:

Back 48

lack of (or) non-functional C1INH (C1 esterase inhibitor)

normally prevents non-specific activation of C1

stress
pharyngeal angioedema- life threatening

Front 49

bone marrow transplants have been successful in treating:

Back 49

common gamma chain deficiency (SCID), RAG deficiency, ADA deficiency, DiGeorge’s

Front 50

3 ways secondary autoimmune diseases can be caused

Back 50

malnutrition (developing countries)
malignancy (problems with infections and immunosuppression caused by treatment or disease)
infections (microbe causes- like AIDs)

Front 51

AIDS is caused by:

infects these types of cells:

leads to:

Back 51

HIV

CD4+ TH1 and TH2 cells

opportunistic infections

Front 52

when immunosuppressive therapy is used:

therapies used:

usually hinder:

Back 52

those with autoimmune diseases

those receiving transplants

corticosterioids, cyclosporin A, FK506, rapamycin

stop T cell-mediated responses more than B cell responses

Front 53

how does cyclosporin A work?

Back 53

interferes with Il-2, prevents T-cell activation

Front 54

caused by microbes usually held in check by the immune system but can be life threatening if you're immunocompromised

Back 54

opportunistic infections (can be parasites, virus, bacterial, fungal)

Front 55

4 types of hypersensitivites- which ones are related to antibody?

Back 55

I- allergic/anaphylactic reaction
II- cytotoxic
III- immune complex disease
IV- cell-mediated delayed hypersensitivity

1st 3 are Ab related

Front 56

Type I hypersensitivity Ab:
Ab increase can be induced by this factor:
antigen often called:
common allergens:

Back 56

IgE
IL-4
allergen
inhaled, injected, ingested

Front 57

3 features of inhaled allergens that promote priming of TH2 --> IgE release

Back 57

molecular type- proteins, because they only induce T cell response
low dose- favors IL-4 producing T-cells
high solubility- allergen is readily eluted from particle

Front 58

IgE half life

what does it attach to, how, and how long?

leads to:

Back 58

2 1/2 days

binds to basophils and mast cells through Fc receptor with high affinity- can last for months

sensitized to allergen held by IgE, activation of mast cells/ basophils

Front 59

3 effects of mast cell activation and granule release

what else can interact with mast cells and cause release of mediators?

Back 59

GI tract- diarrhea, vomiting
airways- phlegm, coughing
blood vessels- edema, inflammation, increased lymph flow

anaphylatoxins

Front 60

Mast Cell preformed mediators and their effects:

newly synthesized mediators and their effects:

Back 60

- histamine- capillary dilation, vascular permeability, smooth muscle contraction
- ECF-A- eosinophil chemotactic factor of anaphylaxis

Newly synthesized:
Leukotrienes- similar to histamine, but even stronger

Front 61

atopic/ local anaphylaxis

systemic anyaphylaxis

genetic component?

Back 61

allergic rhinitis (genetic)
asthma (genetic)

anaphylactic shock= no genetic component

Front 62

in chronic asthma, what cell is involved

Back 62

eosinophils- damage airway

Front 63

clinical features of anaphylactic shock

occurs how quickly:
symptoms in these body areas:
death can be caused by:
occur due to systemic release of:

Back 63

matter of minutes
cardiovascular, respiratory, GI
death: laryngeal edema, respiratory failure, shock
histamine and leukotrienes

Front 64

allergy treatment

local:
systemic:

Back 64

antihistamine

epinephrine (opposite effect of histamine, in epi-pens)

Front 65

IgE immediate reaction time seen/ late phase:
type III arthus reaction time:
type IV delayed reaction time:
granuloma reaction time:

Back 65

<30 min/ 5 hours
5-6 hrs
24-72 hrs
21-28 days

Front 66

how does hyposensitization work?

Back 66

- slowly administer allergen to patient
- decrease IgE, increase IgG response
- IgG out competes IgE

Front 67

3 examples of type II sensitivities

Back 67

1. blood transfusion reaction: type A blood given to type B person
2. drug reactions: drug can be hapten, interact with surface protein of cells, induce Ab response
3. autoimmune hemolytic anemia: patient develops Ab against own RBCs

Front 68

Abs involved in type II sensitivities

how do they work?

Back 68

IgM and IgG (complement activators)

Abs bind to hapten on RBC, lead to cell lysis or phagocytosis via complement

Front 69

how do type III sensitivities work?

Abs involved

Back 69

Soluble Ag-Ab complexes circulate throughout the blood stream, settle in certain target organs (kidney) initiating inflammatory response

IgM or IgG

Front 70

the arthus reaction is _______ induced

Abs are _________, creates Ag-AB complex

can activate ____ cells

site of rxn

will see reaction start in ________ time frame

Back 70

locally

Abs are introduced (Ag already there)

mast cells --> degranulation --> inflammation

on skin

6 hrs

Front 71

common causes of arthus reactions

Back 71

vaccines
insect stings
oral bacteria

Front 72

major organ targets for systemic type III sensitivities

Back 72

kidneys, joints, heart

Front 73

serum sickness

permanent?

Back 73

given large does of Antigen (caused by drugs)
complexes settle in your joints(arthritis), kidney (nephritis), heart (vasculitis)
accompanied by fever

no

Front 74

3 types of diseases associated with type III hypersensitivities

Back 74

infectious/post infectious disease

autoimmune disease (lupus)

drug reactions (serum sickness)

Front 75

how are complexes removed?
what cells destroy them?
works for which Ig:
what Ig type does this not work for?

Back 75

activate complement
stick to complement receptors on RBCs
taken to KUPFFER in liver to remove/destroy

works well for IgM/IgG bc they activate complement
not good for IgA (tend to settle in organs)

Front 76

type IV hypersensitivities

site:
cells often involved:
time of rxn:
sometimes involve ______ which can activate CD8 T cells

Back 76

skin
TH1 --> cytokines they produce
24-78 hrs
can involve haptens soluble enough to bind MHC class I and elicit CD8 T cells response

Front 77

3 examples of type IV hypersensitivities

how is it tested for?

Back 77

1) tuberculin rxn
2) contact dermatitis
3) contact stomatitis (ex. cinnamon)

patch test- contains haptens that could create response, leave on for 72 hrs, see response

Front 78

released by TH1 TCell in type IV

Back 78

chemokines
IFN-gamma
TNF-alpha & LT (cytotoxins)

Front 79

2 phases of type IV hypersensitivity

Back 79

1) sensitization
- hapten makes complex with carrier
- picked up/ presented by dendritic cell

2) elicitation phase
- effector cells CD4 T cells release cytokines
- give response after 24-72 hrs

Front 80

granuloma is made up of macrophages that have turned into _________ and _______

surrounded by ________

eventually causes death of cells in center of granuloma by

Back 80

epithelioid

giant multi-nucleated cells

T-cells

circulation being cut-off

Front 81

autoimmunity vs. autoimmune disease

Back 81

response to self-antigen =not harmful

vs. loss of tolerance = harmful

Front 82

5 mechanisms that contribute to immunological self-tolerance

Back 82

1) negative selection in BM and thymus
2) expression of tissue specific proteins in thymus
3) sequestered Ags (no lymphocyte access)
4) suppression of autoimmune response by Treg cells
5) induction of anergy in autoreactive B/T cells

Front 83

T regulatory cell surface markers

how does it work?

Back 83

CD4
FoxP3
CD25

binds to same APC that autoreactive T-cell is attached to

Front 84

what happens to autoreactive B cells in periphery

Back 84

bind to autoantigen --> are retained in T-cell area of secondary lymphoid structures --> no T cell help --> die

peripheral tolerance

Front 85

gender that autoimmune diseases are more prevalent in

Back 85

females

Front 86

possible causes of autoimmune diseases

Back 86

1) molecular mimicry
2) breakdown in lymphatic regulation
3) microbes *association but causal not proven*
4) sequestered antigens
5) genetic
6) environmental

Front 87

when antigens are shared by humans and microbes aka cross-reacting antigens

example

Back 87

molecular mimicry

- body response to streptococcus
- some Abs will cross-react with myocardial antigen
- rheumatic fever

Front 88

Antigens not exposed to the immune system during immunological development. How might these induce an immune response?

example?

Back 88

sequestered antigens

if there is tissue damage, Ag might be exposed

sympathetic ophthalmia: damage to one eye leads to release of ntraocular protein antigens --> T cells activated --> attacks both eyes

Front 89

example of a genetic autoimmune disease?

what immune cell component does it involve?

Back 89

ankylosing spondylitis

HLA-B27

Front 90

rheumatoid arthritis increases with age due to:

Back 90

involution of thymus and less regulatory T cells

Front 91

5 organ specific type II hypersensitivity diseases and causes

Back 91

Hasmimoto's thyroiditis

pemphigus vulgaris: Abs to intercellular substance of the epithelium (ECM)

benign mucous membrane pemphigoid: Abs to basement membrane

autoimmune hemolytic anemia: Abs to RBCs

myasthenia gravis: Abs to acetycholine receptors

Front 92

3 pathways to destruction in autoimmune hemolytic anemia

Back 92

FcR positive cells in spleen

complement activation in spleen (cells with complement receptor)

complement activation and intravascular hemolysis

Front 93

how can a fetus be affected by myasthenia gravis?

would a fetus be affected by Cell-mediated autoimmundisease from mom?

Back 93

baby would get maternal IgG against AChR, eventually get better because the IgG wouldn't last

No- lymphocytes (Tcells) don't cross the placenta

Front 94

non-organ specific (type III) disease we need to know

organs involved

Back 94

systemic lupus

kidney, heart, CN system

complexes causing inflammatory response

Front 95

systemic lupus erythramatosus

makes Abs against (5):

consequences (3):

Back 95

DNA, ribosomes, histones, snRNP, scRNP

glomerulonephritis, vasculitis, nephritis

Front 96

T-cell mediated autoimmune disease we need to know (type IV)

autoantigen:
consequence:
what type of T-cell?

Back 96

type I diabetes

pancreatic B-cell antigen

Beta-cell destruction = no insulin

CD8 cytotoxic

Front 97

3 rheumatic diseases caused by autoimmunity

Back 97

systemic lupus erythematomus

rheumatoid arthritis

ankylosing spondylitis

Front 98

definition of passive acquired immunity and two types

pros?
cons?

Back 98

administration of preformed antibodies

natural: placental transfer

artificial: anti-toxins, human gammaglobulin

pros: cheap, quick acting
cons: IMMUNITY IS LIMITED

Front 99

definition of active acquired immunity and two types

Back 99

when exposed to the microbe or its products

natural: develops after recovering form an infection

artificial: toxoids, inactivated or killed vaccines, live attenuated vaccines

Front 100

vaccine type for each disease

BCG (tuberculosis)
diphtheria
Hep B
influenza
measles

Back 100

TB: live, attenuated
diphtheria: toxoid
Hep B: recombinant viral protein
influenza: inactivated virus
measles: live, attenuated

Front 101

what do adjuvants do?

2 ways they do it:

ex.

Back 101

non-specifically enhance the immune response

1. prolong exposure to Ag
2. initiating an inflammatory response at the site of innoculation

ex. ALUM

Front 102

killed vs. live vaccines

Ag mass:
duration of immunity:
immunodeficient patient

Back 102

small/ large due to proliferation of microbe
short-lived booster/ often life-long
usually OK/ risk of disseminated disease often

Front 103

why is Alum important?

composed of:

mechanism of action:

Back 103

it's an adjuvant used in the hepatitis B vaccine

aluminum hydroxide gel

delays release of Ag, enhanced macrophage uptake

Front 104

autograft:
isograft:
allograft:
xenograft:

Back 104

same person
identical twin
same species, different genetics
different species

Front 105

two types of graft rejections

Back 105

acute: usually mediated by T cells- takes, then turns black later

hyperacute: Ab-mediated, recipient has Abs to donor organ [immediate rejection] looks white- no vascularization at all

Front 106

occurs when donor lymphocytes in the donor graft attack recipient cells

major problem for:

Back 106

graft vs. host disease (GVHD)

bone marrow transplants

opposite of transplant rejection

Front 107

blood transfusion reactions are examples of ______ hypersensitivity

occur when you have a _____ or ____ incompatability

Back 107

type II- cytotoxic

ABO or Rh

Front 108

85% of people are Rh (+ or -)

type of antibody associated with Rh

type of antibody associated with ABO typing

Back 108

Rh+

IgG (has potential to cross placenta)

IgM

Front 109

one of the most prevalent mucosal diseases in the world

causes an increase in what factor?

Back 109

recurrent aphthous stomatitis (canker sores)

TNF-alpha

Front 110

in pemphigus vulgaris, antibodies are produced against this protein

Back 110

desmoglein 3

Front 111

autoimmune disorder directed against exocrine glands particular salivary (________) and lacrimal glands (____________)

Back 111

Sjogrens syndrome

xerostomia

keratoconjunctivitis sicca

Front 112

generally caused by allogenic bone marrow transplantation

how many per year?

Back 112

graft vs host disease

>4,000/year

Front 113

used to detect autoantibodies in tissue (direct/indirect) or seurm (direct/indirect)

Back 113

immunofluorescence for autoimmune disease
tissue = direct
serum = indirect

Front 114

plasma cell dycrasias

2 examples

Back 114

group of disorders where there is an abnormal proliferation of a clone Ig secreting cells (usually plasma cells) resulting in the production of monoclonal antibody (M protein)

multiple myeloma and wadenstroms macrogloulinemia

Front 115

what is an M protein?

how do we test for its presence?

Back 115

a monoclonal antibody (created in plasma cell dycrasias)

serum protein electrophoresis [SPE]

Front 116

symptoms of multiple myeloma

Back 116

bone pain, recurrent infections, mandible involved first, punched out lesions

Front 117

test to differentiate between a benign granuloma from a myeloma lesion

Back 117

test for kappa and lambda light chain via immunohistochemical staining

all kappa or all lambda: myeloma lesion
a mix of kappa and lambda: benign granuloma

Front 118

Ig associated with wadenstroms macroglobulinemia
leads to ________ syndrome

symptoms seen:

treated with:

Back 118

IgM
leads to hyperviscosity syndrome [build up of IgM in blood stream]

oozing of blood from mucosa, nose bleeding, prolonged bleeding from surgeries, disturbance of vision

treated with plasmaphoresis [thins out blood]

Front 119

technique to differentiate between pemphigus and pemphigoid (type ___ sensitivities)

what are the patterns of each?

Back 119

immunofluorescence: use f-Ab against auto-antibody to tell where it's localized (type II)

pemphigus: chicken wire in epithelium
pemphigoid: linear appearance at basement membrane

Front 120

immunofluorescence that shows a bumpy pattern along the basement membrane is characteristic of what disease? what type of hypersensitivity?

Back 120

systemic lupus erythamatosus
type III

Front 121

concentration of IgM and IgD in

immature B cells leaving the BM

immature B cells after alternative splicing

mature naiive B cells

Ag activated lymphocyte

Back 121

IgM only

IgM (high) IgD (low)

IgM (low) IgD (high)

IgM only

Front 122

two reversible steps of B-cell receptor/Ab production

Back 122

transcription activation with coexpression of surface IgD and IgM

synthesis changes from membrane Ig to secreted

Front 123

when does B Cell receptor editing occur and to what?

Back 123

in BM if it's autoreactive- edits the light chain

Front 124

present on the surface of central memory cell that isn't on the surface of effector memory cells

Back 124

CCR7

Front 125

distinctive features of the mucosal immune system

anatomical features (3)

effector mechanisms (2)

immunoregulatory environment (2)

Back 125

1. intimate interaction between epithelium and lymphoid tissue
2. discrete compartments of diffuse lymphoid tissue and more organized structures such as peyer's patches
3. specialized Ag uptake provided by M cells

1. activated effector T cells predominate even in the absence of infection
2. plasma cells in tissues where Abs are needed

1. active downregulation of inflammatory immune response to food/innocuous antigens
2. inhibitory macrophages and tolerance-inducing dendritic cells