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Microbiology & Immunology > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

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?

25
What do TH1 cells do?
* 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
What does IL-12 do? What induces its production?
* 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
What do TH2 cells do?
* 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
How do TH1 and TH2 cells regulate each other?
* TH2 cells secrete **TGF-ß** and **IL-10** which **inhibit** TH1 cells**​** * TH1 cells secrete **IFN-gamma** which **inhibits** proliferation of TH2 cells
29
How does T helper cell subtyping affect leprosy lesions?
* TH1 response: tuberculoid leprosy * TH2 response: lepromatous leprosy
30
What are the possible steps for naive CD8+ T cell activation to effector TCTL?
* 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
What surface molecules do activated TCTL need to kill infected target cells?
* ONLY CD8/TCR, no costimulation required
32
What are the ways activated TCTL kill target cells?
* 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
What is a T-dependent (TD) antigen?
any antigen with a protein component that can be presented by class II MHC
34
What are the steps for B cell activation by TD antigens (both initially and later with TH2 help)?
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
Describe the B cell co-receptor.
* structure: CD21 (CR2), CD19, CD81 (TAPA-1) * binds to C3d opsonin on antigen * functionally similar to CD4/CD8 * augments signals from BCR
36
Describe the signaling cascade of naive B cell activation.
* 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
How is antibody isotype switching carried out?
* 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
How is affinity maturation carried out?
* 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
What are the differences in primary and secondary antibody response to antigen?
* 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
What is an T-independent (TI) antigen?
* 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
What are the steps for B cell activation by TI antigens?
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
What is the clinical relevance of TI B cell response?
* 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
What is the distribution of antibody isotypes throughout the body?
* IgM: only in blood * IgG & monomeric IgA: in blood and EC spaces * dimeric IgA: mucosal spaces * IgE: epithelial surfaces
44
How is IgA transported into mucosal spaces?
* 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
How is IgG transported and into what tissues?
* **FcRB receptor** * across the **placenta ** * across **endothelium** into the **extracellular spaces**
46
What are the antibody effector functions?
* 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
What do Fc-gamma receptors do?
* 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
What do Fc-epsilon receptors do?
* 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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