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Immunity, Infection and Disease > T-cell and Humoral Effector Mechanisms > Flashcards

T-cell and Humoral Effector Mechanisms Flashcards

1
Q

Individuals tending toward Th2 responses are more vulnerable to what type of infection?

A

Mycobacterial infection

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2
Q

Decreased expression of what causes T cells to migrate from high endothelial venules to lymph node?

A

CD62L (aka L-selectin)

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3
Q

What integrins do T-cells express and to what does each bind?

A

B1 integrin (VLA-4 which binds with VCAM-1) and B2 integrin (LFA-1 which binds with ICAM-1)

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4
Q

Antigen-specific activation of T cells upregulates what integrin and what does this do?

A

VLA integrins. Adheres T-cell to ECM to keep it from recirculating

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5
Q

What types of T-cells release IFNg?

A

CD8+ and (some) CD4+

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6
Q

What types of T-cells release TNF-a?

A

Some CD8s, some TH1s, and some TH2s

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7
Q

What cytokine is a potent macrophage activator and leads to NO production?

A

TNF-a

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8
Q

Whether IL-4 enhances or inhibits an immune response depends on the APC in use. In the case of which APC does it enhance immune response and which does it inhibit?

A

Enhances if B-cells are presenting, inhibits if Macrophages are presenting

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9
Q

GM-CSF

A

Granulocyte Colony Stimulating Factor. Stimulates WBC growth in bone marrow, is able to act over long distance for a cytokine

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10
Q

Three major cytotoxins stored in CD8+ cell granules

A

Perforin, Granzyme, and Granulysin (antimicrobial, apoptosis induction at high conc)

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11
Q

Name three cytokines who are limited to local action due to highly unstable mRNA

A

IL-2, IL-4 and IFN-g

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12
Q

What complement protein is Perforin analogous to?

A

C9

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13
Q

Another name for Fas

A

CD95

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14
Q

Is cell killing with Fas caspase-dependent or caspase-independent?

A

Caspase dependent (activates Caspase 8)

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15
Q

Lymphotoxin-alpha

A

A member of the TNF family, released by CD8+ T-cells to activate macrophages

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16
Q

Are mycobacteria typically processed by the MHC class I or MHC class II pathway?

A

Class II

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17
Q

What type of T-cell do macrophages use MHC class II to present their ingested peptides to?

A

Th1 (Type 1 CD4+)

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18
Q

What two things do Th1 cells do to pump up a macrophage which has ingested antigen to destroy it? (RAMPAGE!)

A

Release IFNg and stimulate the macrophage CD40 with CD40L

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19
Q

What do partially activated macrophages do to get T cells to completely activate them?

A

Secrete IL-12, which skews response toward Th1 (which activate the macrophage) and secrete IFNg (which further activates them)

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20
Q

What are the two forms of leprosy, which is bad, and what determines if someone has one course or the other?

A

Tuberculoid (not so bad) and Lepromatous (bad). People skewed toward Th2 responses (insufficient macrophage activation) have lepromatous

21
Q

For each of the following give the mechanism it has devised to obfuscate the T cell response: mycobacteria, HSV, CMV, EBV, Poxviruses

A

Mycobacteria - inhibits phagosome fusion, HSV - ICP47 blocks TAP, CMV - targets MHC I for degradation, EBV - blocks proteasome and produces its own IL-10, Poxviruses - produces CR that block cytokine signals

22
Q

Two molecules expressed in both effector and memory T cells, and two molecules expressed in both naive and memory T cells

A

Effector and Memory - CD44 (adhesion) and IFNg, Naive and Memory - CD45RA (modulates T cell signaling) and CD127 (part of IL-7 receptor)

23
Q

Two types of Memory T cells and some distinguishing features of each

A

Effector Memory (do not express CCR7, express integrin and chemokine receptors, secrete IFNg, IL-4 and IL-5 after restim) and Central Memory (express CCR7, secrete less cytokines)

24
Q

Give a brief moniker which describes each of the 5 immunoglobulin isotypes

A

IgD - membrane only, IgG - jack of all trades, IgM - produced first, activates classical complement, IgA - mucosal secretions, neutralize microbes and toxins, IgE - parasites, allergy

25
Q

What Ig isotypes are primarily responsible for opsonization?

A

IgG1 and IgG3 by binding IgG Fcg1 receptor (CD64) on neutrophils and macrophages

26
Q

What receptor on NK cells allows for ADCC (antibody dependent cell-mediated cytotoxicity)?

A

FcgRIII (CD16)

27
Q

What type of pathogens stimulate IgG production? IgE production?

A

IgG - bacteria and viruses, IgE - helminths

28
Q

What does the Poly-Ig receptor transport and from where to where?

A

IgA molecules into the lumen (respiratory, GI, etc) to defend even before mucosal barrier

29
Q

What is the most abundant antibody produced in the adult human?

A

IgA

30
Q

What transports antibodies from mother to fetus and what type of antibodies does it transport?

A

Neonatal Fc receptor (FcRn). Transports IgG

31
Q

What role does the FcRn play after birth?

A

In the newborn it absorbs IgG in the breastmilk in the intestine and transports it across gut into circulation

32
Q

Which complement pathways are adaptive and which are innate?

A

Classical is adaptive, Mannose and Alternative are innate

33
Q

Three main outcomes of complement activation

A

MAC formation, recruitment and activation of inflammatory cells, opsonization

34
Q

What causes activation of the alternative complement pathway?

A

Stabilization of spontaneously activated component by PATHOGEN SURFACES

35
Q

Composition of the complement molecule C1

A

6 C1q subunits, 1 C1r and 1 C1s

36
Q

What part of C1 binds adjacent antibody complexes and what is the result of this?

A

C1q. Result is activation of C1r which cleaves and activates C1s, which cleaves C4 to C4b and C4a, and cleaves C2 to C2b and C2a

37
Q

After activated C1s cleaves C4 to C4b and C4a, and C2 to C2a and C2b what happens?

A

C4b deposits on the membrane and binds C2b. The two together become a C3 convertase

38
Q

What is the composition of the C3 convertase in the classical pathway?

A

C2b and C4b (they also associate with the C3b they are cleaving)

39
Q

What is the first step in the alternative complement pathway?

A

Spontaneous hydrolysis of C3

40
Q

What molecule does spontaneously hydrolyzed C3 bind to and what is the result of this binding?

A

Factor B, which then gets cleaved to Bb and Ba by Factor D

41
Q

What is the composition of the C3 convertase in the alternative complement pathway?

A

C3(H2O) and Bb (note that C3(H20) denotes hydrolyzed C3)

42
Q

Spontaneous hydrolysis of C3 begins the alternative pathway. Why doesnt this pathway run rampant?

A

Freed C3b is rapidly inactivated unless it binds to a pathogen cell surface

43
Q

What is the composition of the C5 convertase in the alternative pathway?

A

2 C3b and 1 Bb. It is stabilized by factor P binding

44
Q

What is the composition of the C5 convertase in the classical pathway?

A

C4b, C2b, and C3b

45
Q

What general principal governs a and b molecules in complement cascades?

A

A molecules are smaller molecules which diffuse away and have other effects (eg anaphalytoxins), and b molecules are larger and continue the cascade (eventually forming the MAC)

46
Q

In both the classical and alternative complement pathways, what is the sequence once C5b has been generated?

A

C6 binds C5b, which recruits c7, which recruits C8, which recruits many C9s that insert into membrane forming a pore (MAC)

47
Q

Four molecules on host cell surfaces that inactivate complement complexes

A

MCP/CD46, Decay Accelerating Factor (DAF), CD59, Complement Receptor 1 (CR1)

48
Q

Four serum soluble molecules that inactivate complement complexes

A

C1 inhibitor, Factor I, Factor H, C4 binding protein

49
Q

What surfaces are most suitable for binding of Factor P (which stabilizes C3bBb complement complexes)

A

Microbial surfaces

Immunity, Infection and Disease (86 decks)

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