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Microbiology & Immunology > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

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1
Q

Define adaptive immunity.

A

specific lymphocyte response to foreign antigen, which includes the development of immunological memory

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2
Q

What are the humoral and cellular mediators?

A
  • humoral: antibodies
  • cellular: lymphocytes
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3
Q

Define clonal selection.

A

process by which lymphocytes are activated and expanded by encounter with antigen that is specifically recognized by the TCR/BCR

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4
Q

What do CD4+ T cells do?

A
  • helper T cells
  • direct and facilitate adaptive and innate immune responses
  • “director” of the adaptive immune response
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5
Q

What do CD8+ T cells do?

A
  • cytotoxic T cells
  • kill cells infected with intracellular pathogens
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6
Q

What do B cells do?

A
  • produce antibodies
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7
Q

What are the steps for naive CD4+ T cell activation to effector T cell?

A
  1. APC presents MHC+peptide which is recognized by TCR
  2. co-stimulation by CD28-B7 interaction
  3. transcription factors are made, IL-2 is produced
  4. IL-2 acts on the secreting cell, initates T cell proliferation and effector functions
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8
Q

Describe the signaling cascade of naive CD4+ T cell activation.

A
  1. antigen peptide + MHC is recognized by TCR
  2. tyrosine phosphorylation of ITAMs on CD3 and zeta-chains
  3. ZAP-70 binds to zeta chains
  4. results in 3 cascades leading to transcription factors, all required for IL-2 production
    1. **NFAT **
    2. NF-kB
    3. AP-1
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9
Q

What happens when TCR signaling is blocked?

A
  • IL-2 generation & T cell response inactivated
    • CD4+ T cells will not provide T cell help
    • CD8+ T cells will not kill intracellular pathogens
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10
Q

What do cyclosporin A (CsA) and FK-506 (tacrolimus) do?

A
  • Immunosupressive Drugs: inhibit the activity of calcineurin
    • ​direct: blocks activation of NFAT
    • consequence: blocks synthesis of IL-2
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11
Q

What does Rapamycin (sirolimus) do?

A
  • Immunosuppresive drug: inhibits signaling from IL-2 receptor
    • Direct: blocks p70S6 kinase involved downstream of IL-2 signaling
    • Consequence: blocks T cell proliferation and acquisition of effector functions
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12
Q

What is ZAP-70 deficiency? What is its molecular basis? Symptoms?

A
  • autosomal recessive immunodeficiency disease, SCID
  • lack of ZAP-70 results in complete lack of CD8+ T cells and CD4+ T cells are non functional
  • Symptoms: frequent infections, failure to thrive
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13
Q

What is a mitogen? Examples?

A

substance that stimulates proliferation of T and B cells

ex. bacterial superantigens, mitogenic lectins, pharmacological activators

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14
Q

How do bacterial superantigens (sAG) work? What’s their clinical relevance?

A
  • act as glue between TCR Vß region and non-polymorphic region of MHC protein
    • TCR: specific Vß but any antigen specificity allowed
    • MHC: Class II, any peptide allowed
  • activate up to 1/5 of T cells in body, results in massive release of cytokines and moderate to severe illness
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15
Q

What are some examples of sAg? Symptoms?

A
  • Toxic Shock Syndrome
    • pathogen: Staphylococcus aureus superantigen (TSST-1)
    • symptoms: hypotension, organ failure, fever
  • S. aureus food poisoning
    • pathogen: S. aureus enterotoxins (SEA, SEB, SEC, SED, SEE)
    • symptoms: food poisoning effects
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16
Q

How do mitogenic lectins work? Examples? Usefulness?

A
  • plant-derived carbohydrate-binding proteins that crosslink T cell surface receptors, mimicking antigen stimulation; does not require APCs
  • examples:
    • T Cells:
      • concanavalin A (ConA)
      • phytohemagglutinin (PHA)
    • T & B Cells:
      • pokeweed mitogen (PWM)
  • useful for in vitro T cell activation (funcitonal assays)
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17
Q

How do pharmacological stimulators work? Example? Usefulness?

A
  • bypass TCR & APCs for T cell activation; activates transcription factors for IL-2 production
  • phorbol myristate acetate (PMA) with ionomycin
    • ​PMA: activates NF-kB and AP-1
    • ionomycin: activates NFAT
  • useful for in vitro T cell activation (funtional assays)
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18
Q

OVERVIEW:

How do antigen-specific CD4+ T cells find APCs presenting the appropriate stimulatory peptide+MHC & become activated?

A
  • antigen is captured in lymphatic system via LNs or spleen
  • naive T cells circulate between LNs and spleen searching for the antigen presented by APCs
  • Signal 1: APC presenting correct MHC-II + peptide bind to CD4/TCR on the T helper cell
  • Signal 2: Co-stimulation occurs via CD28 on T cell and **B7 **on APC
  • signaling cascade results in IL-2 production
  • T cells proliferate and become effector or memory cells in the periphery
  • T cells look for their antigen presented in vascular endothelial cells via MHC-II and bind to those cells via **VFA-1 : VCAM-1 **interaction
  • T cells move into periphery to site of inflammation
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19
Q

How do naive T cells gain entry into LNs/ spleen?

A
  • naive T cell enter HEVs in LN, attach to endothelial cells & undergo diapedesis
  • surface molecules
    • naive T cells: L-selectin, LFA-1
    • endothelial cells: GlyCAM-1/CD34,ICAM-1, (& cytokines on ECM)
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20
Q

How do activated effector/memory T cells gain entry to periphery?

A
  • activated T cells exit LN in efferent lymph and collect in thoracic duct
  • surface molecules: change so T cells can ciruclate between blood and sites of peripheral inflammation
    • effector T cells: LFA-1,** VLA-4**, (Low L-selectin)
    • vascular endothelial cell: ICAM-1, VCAM-1
21
Q

What is the expression pattern of peripheral tissue endothelial adhesion molecules during an immune response?

A
  1. ​immediately: E-selectin, recruits neutrophils
  2. 24 hrs: ICAM-1, recruits monocytes
  3. 24-48 hrs: VCAM-1, recruits activated effector T cells
22
Q

Compare naive (CD4+ and CD8+) T cells vs. activated T cells.

A
  • naive T cells:
    • migrate from blood to LNs
    • High L-selectin : Glycam-1/CD34
    • **LFA-1 **: ICAM-1
  • activated T cells:
    • migrate from blood to inflammed peripheral tissues
    • High VFA-4 : VCAM-1
    • **LFA-1 **: ICAM-1
23
Q

What are the characteristics of a memory T cell?

A
  • does not require co-stimulation for activation
  • can turn into effector T cell in hours (must faster than primary response in naive T cells)
  • long-lived
  • gradually lost with age (i.e. shingles- varicella zoster virus)
24
Q

What are two subsets of CD4+ TH cells?

A
  • TH1
  • TH2
25
Q

What do TH1 cells do?

A
  • provide help to macrophages & CD8+ T cells
  • produce IFN-gamma and upregulate surface CD40L
    • ​stimulates macrophages to kill intracellular bacteria
    • stimulates CD8+ T cell activation via Pathway 3
26
Q

What does IL-12 do? What induces its production?

A
  • drives differentiation of naive CD4+ T cell to TH1 subtype along with IFN-gamma produced by NK cells
  • produced by DCs and macs in response to viruses and some bacteria
27
Q

What do TH2 cells do?

A
  • provides help to B Cells
  • produces IL-4, IL-5, IL-6 and upregulates surface CD40L
    • ​stimulates B cell proliferation and differentiation to antibody-secreting plasma cells
  • critical for immune response to certain parasites (i.e. worms) and responsible for immunpathologies such as allergies and asthma thru **Ig class switching **
28
Q

How do TH1 and TH2 cells regulate each other?

A
  • TH2 cells secrete TGF-ß and IL-10 which inhibit TH1 cells​
  • TH1 cells secrete IFN-gamma which inhibits proliferation of TH2 cells
29
Q

How does T helper cell subtyping affect leprosy lesions?

A
  • TH1 response: tuberculoid leprosy
  • TH2 response: lepromatous leprosy
30
Q

What are the possible steps for naive CD8+ T cell activation to effector TCTL?

A
  • Pathway 1: directly stimulated by DCs in high inflammatory environment
    • activated DCs have lots of B7, migrate to LNs
    • DCs directly activate CD8+ T cell via MHC-I: TCR and B7: CD28
  • Pathway 2: stimulated by DCs activated by CD4+ T cells
    • activated DCs migrate to LN and activate CD4+ T cells via MHC-II: TCR and CD40: CD40L
    • DCs become more activated and produce more B7 to activate CD8+ T cell
  • Pathway 3: stimulated by IL-2 from CD4+ T cells activated by DCs
    • CD4+ T cell is activated by DC to produce IL-2
    • IL-2 binds to IL-2R on CD8+ T cell to activate it
31
Q

What surface molecules do activated TCTLneed to kill infected target cells?

A
  • ONLY CD8/TCR, no costimulation required
32
Q

What are the ways activated TCTL kill target cells?

A
  • release cytolytic granules into immunological synapse which leads to target cell apoptosis
  • Fas-L on TCTL interacts with Fas on target cell to induce apoptosis
33
Q

What is a T-dependent (TD) antigen?

A

any antigen with a protein component that can be presented by class II MHC

34
Q

What are the steps for B cell activation by TD antigens (both initially and later with TH2 help)?

A
  1. B cells enter LNs or spleen and bind to native antigens via BCR (not processed peptides)
  2. BCR crosslinking by multivalent antigen (repeated epitopes)
    signaling cascade –> transcription factors are made
    B cell proliferation, autocrine cytokine secretion, and IgM secretion
  3. BCR binds to antigen and internalizes it
  4. —continues w/ TH2 help—
  5. B cell presents antigen peptide via MHC-II and B7 co-stimulator to TH2 cell
  6. CD40L upregulation is induced in TH2 from specific antigen recognition, binds to CD40 on B cell
  7. cytokines IL-4, IL-5, IL-6 produced by TH2
  8. B cell differentiation:
    1. Ig class switching (non-IgM)
    2. affinity maturation (somatic hypermutation)
35
Q

Describe the B cell co-receptor.

A
  • structure: CD21 (CR2), CD19, CD81 (TAPA-1)
  • binds to C3d opsonin on antigen
  • functionally similar to CD4/CD8
    • augments signals from BCR
36
Q

Describe the signaling cascade of naive B cell activation.

A
  • BCR crosslinking by multivalent antigen
  • ITAMS on Ig-alpha and Ig-beta BCR are phosphorylated
  • Syk kinase binds to Ig-alpha and Ig-beta
  • results in 3 cascades leading to transcription factors, all required for B cell proliferation, autocrine cytokine secretion, and IgM secretion
    • NFAT
    • NF-kB
    • AP-1
37
Q

How is antibody isotype switching carried out?

A
  • occurs in mature B cells in secondary lymphoid tissues w/ TH2 help
  • specific isotypes stimulated by specific cytokines
    • ex. IgA stimulated by IL-5
38
Q

How is affinity maturation carried out?

A
  • occurs in germinal centers in secondary lymphoid tissues
  • B cells interact with TH2 cells, mature, and proliferate and undergo somatic hypermutation
    • variable regions in Ig undergo random mutations
  • mutated BCRs interact with follicular DCs bound to antigen
    • high affinity B cells become antibody-secreting plasma and memory B cells
    • low affinity B cells undergo apoptosis
39
Q

What are the differences in primary and secondary antibody response to antigen?

A
  • primary: no pre-formed antigen-specific B cells made
    • significant lag time
    • modest antibody titer
  • secondary: memory B cells already made
    • shorter response time
    • higher antibody titer (particularly IgG)
40
Q

What is an T-independent (TI) antigen?

A
  • carbohydrate antigens that provoke an antibody response independent of CD4+ T cells
  • cannot be presented by class II MHC, so T cells cannot respond to pure carbohydrate antigen
  • ex. polysaccharide encapsulated bacteria
41
Q

What are the steps for B cell activation by TI antigens?

A
  1. carried out by B-1 cells early in development
    • express CD5
  2. BCR crosslinking by multivalent antigen (highly repetitive carbohydrate epitopes)
  3. strong signaling cascade –> transcription factors are made
  4. B cell proliferation, autocrine cytokine secretion, and IgM secretion
  5. NO T CELL HELP
    • No Ig class switching (only IgM)
    • No affinity maturation (low affinity Ab)
    • No secondary response (no memory B cells)
42
Q

What is the clinical relevance of TI B cell response?

A
  • helpful for making vaccines to encapsulated bacteria
    • conjugate TI carbohydrate Ag to TD “carrier” proteins which can be presented by MHC-II
    • artificially adds T cell help to the response to provoke high-affinity, long-lasting IgG Ab response
    • ex. *H. influenzae *vaccine
  • splenectomized patients w/ B cell immunodeficiency are particularly vulnerable to TI pathogens
43
Q

What is the distribution of antibody isotypes throughout the body?

A
  • IgM: only in blood
  • IgG & monomeric IgA: in blood and EC spaces
  • dimeric IgA: mucosal spaces
  • IgE: epithelial surfaces
44
Q

How is IgA transported into mucosal spaces?

A
  • IgA is transported across epithelial surfaces by **poly-Ig receptor **
  • dimeric IgA taken from basolateral face of epithelial cell (mucosal side) thru poly-Ig receptor and transported accross the cell to apical face (lumen side)
  • at apical face, receptor is cleaved and IgA is bound to mucus thru **secretory piece **
45
Q

How is IgG transported and into what tissues?

A
  • FcRB receptor
  • across the **placenta **
  • across endothelium into the extracellular spaces
46
Q

What are the antibody effector functions?

A
  • Ab bind to surface receptors on pathogens, prevent it from interacting with host cells
  • Constant region of Ab bound to pathogen binds to Fc receptors on host cells, which induces phagocytosis of opsonized pathogen
    • Fc-gamma, Fc-epsilon
47
Q

What do Fc-gamma receptors do?

A
  • bind to IgG constant regions
  • found on macs
    • promote phagocytosis and creation of phagolysosome
  • found on NK cells
    • promote release of lytic granules and cause apoptosis
48
Q

What do Fc-epsilon receptors do?

A
  • bind to IgE constant regions
  • found on Mast cells
    • triggers release of histamine
    • causes asthma and allergy
  • found on eosinophils
    • triggers release of granules
    • combats parasites

Microbiology & Immunology (7 decks)

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