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humoral immune response Flashcards

1
Q

what do resting mature B cells express

A

BCR: IgM, IgD, IgA, IgB

Co-BCR: CD19, CD81, CR2 (CD21)

HLA class II and I

CD40

CD20

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2
Q

what types of B cells are there? what are their subsets (if they have them)?

A

B-2 cells:

  1. folliclur B cells- re circulating be cells- majority
  2. marginal B cells that reside in spleen: bloode-born polysaccharde ags

B-1 cells

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3
Q

migration of naive B cells steps

A
  1. start in primary lymphoid follicles (spleen through blood, lymph nodes via lymphatics)
  2. Antigen- will move to secondary lymphoid tissue through HEV and receive signal from FDCs to survive*. exit through efferent lympathic signal

No antigen- will migrate back to primary follicle (CXCR5) and die within weeks

**there is a competition for survival signals

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4
Q

competition for survival signals

A
  1. B cells will recognize specific ag by their idiotype/paratype
  2. antigen will bind to mlg on naive cells to activate them
  • second signal can occur in T-dependent or T-independent manner- depends on antigen

complete activation requires two signals

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5
Q

what are the steps for the first signal required for competition survival

A
  1. ag recognizes by mlgs through cross linking* 2 or more BCR’s
  2. syk-B cell phosphorylation sends signals to IgA and IgB cytoplasmic tails
  3. prepares cell for second signal, produces transcription proteins? and NF-KB and AP-1

** crosslinking is necessary but not sufficient

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6
Q

what are the steps in crosslinking

A
  1. ag recognizes CR2/CD21
  2. CR2/CD21 provides crosslinkage signaling
  3. signaling occurs through IgA&IgB and cr2&cd19 cytoplasmic tails(BCR)

**if ag is attached to CD3 then the signal will be much stronger

ag can also act as pamp to stimulate tlr which provides same sort of signaling

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7
Q

what are the outcomes of the first signal in compeition survival and what changes in activated be cells do they result from

A
  1. secretion of IgM
  2. increased survival and proliferation—from expression of proteins that promote survival
  3. interaction with helper T cells— from increased B7 exp
  4. responsiveness to cytokines— from increased cytokine receptors
  5. migration from follicle to T cell areas— from increased exp of CCR7
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8
Q

what is the migration of B cells in between the first and second signal and what do they secrete/exp?

A

after activation of ag, B cells change chemokine receptor exp and move to follicular edge

secrete low levels of IgM and increase expression of co stimulatory molecules and cytokine receptors

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9
Q

what are the steps of the T-dependent immune signal? what does this pathway produce?

A
  1. co-stimulatory molecules stimulate signals from CD40L on th cell and CD40 on B cell
  2. induced exp of AID enzyme
  3. class switching and affinity maturation occur due to cytokines being released by T cells

produces isotype-switched, high-affinity antibodies, memory b cells, long-lived plasma cells

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10
Q

what are the two roles of class switching in the germinal center?

A
  1. to induce H chain class switching
  2. to augment B cell differention and proliferation
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11
Q

what are the types of antibodies, what are they activated by to class switch and what are their functions?

A

IgM— first Ig made— complement activation

IgG— ?—opsonization/phagocytosis, complement activation, neonatal immunity

IgE, IgG4— IL-4— helminths immunity, mast cell degranulation

IgA— mucosal tissues, cytokines (TGF-b, etc) mucosal immunity

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12
Q

how does class switching work?

A

CD40:CD40L trigger isotype switching and affinity maturation by:

  • modulation of switch regions
  • increasing accessibility of DNA at specific C region
  • inducing exp of AID
  • rearranged VDJ gene segment recombines with a downstream C region gene and intervening DNA is deleted
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13
Q

what is affinity maturation? what enzyme does it use?

A

point mutations in the variable regions of the Ig genes in order to expand the repertoire for high affinity ag specific antibodies- result of somatic hypermutation

AID is key enzyme. converts Cs to Us allowing Ape 1 to create nicks in strand that lead to double stranded break

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14
Q

what do follicular T helps do? how do they work? where do they work? what do they express? what do they secrete?

A

they provide a selection checkpoint in proliferation

work with FDC’s to interact with high affinity B cells which is critical for B cells survival

provide intact antigen in form of complexes

work in the germinal center- produces highest affinity ab’s

express cd4 and low levels of CD25

secrete IL-21- facilitates differentiation for plasmablasts, provides IFN-y and IL-4 for cytokine switching

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15
Q

what are plasma cells? what do they express? what is it dependent on? what do they secrete?

A

terminally differentiated effector B cells

express CD19, CD20, HLA class II, CD27

dependent on selected Ig (will only produce that kind)

secrete A LOT of ab’s- expand in ER- effector molecules of humoral immunity

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16
Q

what cells are involved in T-independent responses? where are they found? what does this pathway produce?

A

B-1 cells- respond to non-protein ag in mucosal tissues

marginal zone B cells- in spleen recognize blood-borne polysaccarhides

produces mainly IgM, low-affinity ab’s and short lived plasma cells

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17
Q

what do memory B cells do? what do they express? what are they dependent on? what are they capable of?

A

survive for long periods without ag stimulation

express high levels of anti-apoptotic protein BCL-S, also CD27, CD45R(O)

sIg class dependent

capable of mounting a rapid secondary immune response (subsequent exposure to same ag)

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18
Q

what are the two antibody feeback mechanisms? what antibody does these?

A

control mechanism that is triggered by ab’s to block further ab production

BCR signaling leads to PIP3 formation which binds other molecules to activate ab production

Fc receptor associate phosphatase, SHIP, binds to itim, converts PIP3 to PIP2 in bcr which blocks downstream signaling

occurs in IgG only

19
Q

what is humoral immunity?

A

branch of adaptive immunity thats mediated by ab’s which are produced by B cells and plasma cells

principle defense against extracellular pathogens

20
Q

where are ab’s produced? what are they mediated by?

A

produced by the plasma cells in the lymphoid tissues and organs. operate at distant away from production site

mediated by Fc region. different isotypes have different Fc’s

all functions triggered by binding of ag to Fab (v) region

21
Q

what are the effector functions of the adaptive immune system? (7 things)

A
  1. neutralization of microbes and toxins
  2. opsonization and phagocytosis of microbes
  3. ab-dependent cellular cytotoxity
  4. phagocytosis of microbes opsonized through complement system
  5. inflammation
  6. lysis of microbes
  7. complement activation
22
Q

what are the two functions of the Fc region? what does the fc contain?

A
  1. delivers ab’s to inaccessible anatomical sites
  2. link bound antigen to molecules that effect destruction

contains binding sites for complement and Fc receptors

ag bound ab’s will bind to Fc receptors in order to act as opsonins or to activate cells!

23
Q

what are the different fc receptors? what is their affinity level? what cells are they located on? what is their effect?

FYI: CD’s in this case are Fc’s

A

CD64:

  • high
  • macrophages,neutrophils,eosinophils
  • phagocytosis, activation of phagocytes

CD32:

  • low
  • macrophages, neutrophils, eosinophils, platelets
  • phagocytosis, cell activation

CD16:

  • low
  • NK cells
  • ADCC

FCERI:

  • high
  • mast cells, basophils, eosinophils
  • activation (degranulation) of mast cells and basophils
24
Q

how do phagocytes interact with Fc? what ab is involved?

A

phagocytes have Fc receptor that binds to Fc region of antibody (thats attached to ag) or opsonized microbe (in complement)

phagocyte phagocytoses ab:ag complex (will happen quicker if ab aggregates ag) or opsonized microbe (complement) in response to Fc receptors signals

25
Q

what is classical complement?

A

ab-directed mechanism of activation. most effecient and rapid pathway

26
Q

what occurs in the initiation step of complement? what are the structures involved?

A
  • ab (2 IgG or IgM) bound to ag, conformational change, C1 binds to the Fc region
  • C1 made up of two C1r and C1s components bound to one C1q
  • ab:ag complex binds to multiple c1q domains
  • when binding occurs, conformational change happens, which cleaves the C1r and C1s, activating C1qrs complex
27
Q

what are the ways neutralization works? which ab’s do it?

A

ab’s neutralize the infectivity and potential effects of infection

may involve steric hindrance of microbes

  1. ab blocks entry of microbe through epithelial barrier
  2. ab blocks binding of microbe to cell
  3. ab blocks binding of toxin to cellular receptor

any class of ab works- higher affinity the better

28
Q

how is waste from the complement system handled?

A

opsonized microbes from C3b bind to CR1 on erythrocytes

erythrocyte carries immune complexes to spleen or liver where it dettaches and undergoes phagocytosis

29
Q

how does ADCC work?

A

NK cells bind to ab-coated cells (IgG) by Fc receptors (low affinity CD16) and destroy infected cell

30
Q

what is the main therapeutics involving adaptive immune system? how does it work?

A

IVIG for rapid protection after exposure

IVIG also used to treat autoimmune dieases

suppresses immune response by engaging inhibitory fcr on B cells and DC’s

31
Q

what are the two natural antibodies? what is their precursor? what is an example of natural ab?

A

IgM mainly, IgG

produced by B-1 and marginal zone B cells

ex: abo blood groups

32
Q

how does fetus receive immunlogical protection from mother?

A
  • physical barrier from microbes with placenta
  • fetus recieves IgG from mom
  • fetus gets IgA from breast milk
33
Q

what is the mechanism of how fetus receives IgG?

A
  1. IgG leaves blood and binds to FcRn ( found in endothelial cells, macrophages, etc)
  2. complex undergoes endocytosis and translocation into placenta
  3. IgG protected by acidic ph
  4. fcrn recyles it to the cell surface at neutral ph when its done
34
Q

what happens when baby is born?

A

maternally derived IgG is broken down

IgM is produced at birth, IgG and IgA lag 6-12 months leaving a vulnerable period when baby is not immunocompetent

35
Q

what are immunizations and what are the two types? what is vaccination

A

antigenic stimulus that can elicit a specific adaptive immune response and can be recalled during subsequent infections

passive- introduction of an ab or antiserum into naive recipient

active- intro of an ag that provokes an adaptive immune response

vaccination is intentiol delivery of ag

36
Q

how do immunizations work? what is hyper-immunization?

A

mimics a natural infection

normal immune response invoked to destroy and clear components of vaccine

primary response is priming

each subsequent immunization provides a stonger response

hyper-immunization is when continual presentation of ag achieves a heightened state of immunity

37
Q

what is passive immunization? what does it do? what are some ex?

A

immediate but transient immunity, uses preformed ab’s

  1. prevent disease after known exposure
  2. help make symptoms of ongoing disease milder
  3. protect immunosuppressed patients
  4. block action of bacterial toxins and prevent disease that they cause

ex: snake bite venom, passive IgG from mother to child

38
Q

what is active immunization? ex?

A

delayed but more permanent

produces immunological response

ex: natural exposure to pathogens, vaccines

39
Q

what is combined passive-active immunization?

A

designed to give immediate protection as well as more permanent protection

ex: tetanus, rabies

40
Q

criteria for effective vaccine

A
  1. safe
  2. provides protection against pathogen
  3. gives sustained protection
  4. induces neutralizing ab (for cells that can’t be replaced)
  5. induces t cells (for intracellular pathogens)
  6. practical considerations (inexpensive, distributable, easily given)
41
Q

what are some potential problems with vaccines

A
  1. vaccines may not have specific epitope
  2. individual genetics
  3. adverse effects
  4. young and old people
  5. many do not induce cmi, only ab
  6. allergies
42
Q

what are some ways pathogens evade humoral immunity? what bacteria implement them?

A
  1. change of surface ags- many virus (HIV) or bacteria (N gonorrhea)
  2. outer capsule prevents complement activation- many bacteria (N gonorrhea)
  3. capsule prevents binding of abs and phagocytosis- streptococcus
43
Q

what is the cellular sequence of B cell activation

A
  1. recognition of membrane bound IgM or IgD by the epitope
  2. endocytose and process ag to express on surface with class II
  3. travel to T cell zone
  4. T helper cell that has been activated by DC from the same ag will recognize epitope that B cell is presenting in conjugation with CD4
  5. up regulation of B7 on b cell to react with CD28 on T helper cell
  6. T cell reponds reacts with CD40L (on T cell) with CD40 (on B cell)- provides specifity of rxn
  7. T cell releases cytokines to B cells
  8. proliferation of specific B cell clone

* same players at with ag presenting cell

44
Q

where does somatic hypermutation happen

A

hypervariable regions of the light and heavy chains- secondary, tertiary, etc

every time your expised to ag, you make a higher affinity ab to it

point mutations become more specific to epitope

SFM (6 decks)

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