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IHO Mike Rose > Adaptive immunity Exam 2 > Flashcards

Adaptive immunity Exam 2 Flashcards

1
Q

Type 1 Helper T cells (Th1)

A

Recognize antigen and make a lymphokine that attracts thousands of macrophages, to area of antigen recognition.

This intense inflammation can wipe out a serious infection, or a transplanted kidney.

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2
Q

Th17 Helper T cells (Th17)

A

Similar to Th1 in that their main role is to cause focused inflammation, although they are more powerful than Th1.

Have been implicated in many serious forms of autoimmunity.

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3
Q

Type 2 Helper T cells (Th2)

A

Stimulate macrophages to become alternatively activated, able to function in walling-off pathogens and promoting healing.

Process usually takes place after the pathogen-killing Th1 response.

Very important for parasite immunity.

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4
Q

Follicular Helper T cells (Tfh

A

Stimulated by antigen and migrate from T cell areas of lymph nodes into the B cell follicles, where they help B cells get activated and make the IgM, IgG, IgE, and IgA anitbody subclasses.

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5
Q

Regulatory T cells (Treg)

A

Make cytokines that suppress the activation and function of Th1, Th17, and Th2 cells, so they keep the immune response in check.

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6
Q

Cytotoxic T cells (CTL)

A

Destroy any body cell they identify as bearing a foreign or abnormal antigen on its surface.

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7
Q

CD4

A

Marker on all helper T cells’ surfaces which increases their affinity for antigen, helps get them activated.

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8
Q

CD8

A

Marker on all cytotoxic T cells.

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9
Q

General activators of T cells

A

IL-2 and IL-15

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10
Q

Cytokines that drive T helper cells to Th1 subtype

A

IL-12 and IFN-gamma

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11
Q

Cytokines that drive T helper cells to Th2 subtype

A

IL-4

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12
Q

Cytokine that downregulates Th1

A

IL-10

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13
Q

Cytokine that downregulated Th1 and Th2

A

TGF-Beta

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14
Q

FAS

A

Protein on a target cell that T cells bind and induce caspase activation and apoptosis

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15
Q

Toxic agents that can kill affected cells

A

TNF, Perforin, and Granzymes

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16
Q

T cell lymphocyte markers

A

TCR antigen receptor (alpha-beta or gamma-delta), CD3, CD4, CD8, and CD23

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17
Q

B cell lymphocyte markers

A

Immunoglobulin antigen receptor, CD1, CD19, CD20, CD23, CD40, CD79a, CD79b

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18
Q

IgG

A

Most abundant anitbody in the blood

Two adjacent IgG molecules, binding an antigen such as a bacterium, cooperate to activate complement.

Very effective at toxin neutralization. Decent bacterial lysis and antiviral activity.

Some lyse the bacterium. Others diffuse away and attract phagocytic cells, primarily PMNs.

Only class of antibodies that cross placenta.

By far the highest serum concentration and longest half life.

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19
Q

IgM

A

A large polymeric immunoglobulin. Better at activating complement than IgG.

Is first type to appear in the blood after exposure to a new antigen. Replaced by IgG in a week or two.

Very good complement fixation and bacterial lysis. Some antiviral acitivity

Pentamer

Largest Ig.

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20
Q

IgD

A

The main form of anitbody inserted into B cell membranes as their antigen receptor which seems to be its only biological role.

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21
Q

IgA

A

The most important class of antibody in the secretions like saliva, tears, gu and gi fluids, and milk.

Associated w/ another chain called secretory component which it acquires from epithelial cells during the process of being secreted. This makes IgA resistant to digestive enzymes.

Important role in first line of defense against microorganisms trying to gain entry to body through mucous membranes.

Very strong antiviral activity and toxin neutralization.

High amounts in colostrum and breast milk that protects vs. respiratory and GI infx.

Dimer (1-3 monomers)

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22
Q

IgE

A

Designed to attach to mast cells in tissues. When IgE encounters antigen it will cause the mast cell to make prostaglandins, leukotrienes, and cytokines. Also stimulates granule release which contains inflammation mediators like histamine.

These produce the symptoms of allergy, but the real role of IgE is to fight off parasites.

Normally present in very low serum concentrations.

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23
Q

H Chain types

A

Gamma, alpha, mu, epsilon, delta

IgG, IgA, IgM, IgE, and IgD respectively

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24
Q

L chain types

A

Kappa or lambda.

Each cell has option for both, but uses only one.

Not switched when antibodies switch cell types (i.e. IgM to IgA)

25
Q

Hypervariable regions

A

aka complementary-determining regions (CDR).

3 areas of v domain that contain the bulk of the antibody’s variability. These comprise the actual antigen-binding site.

26
Q

Valence

A

The number of antigenic determinants (epitopes) an antibody molecule can theoretically bind.

IgG = 2, IgA = 4, IgM = 10 etc.

27
Q

Isotypes

A

On the basis of slight differences in the amino acid sequences of their H chain C regions the 5 main classes are divided into subclasses:

IgG1, IgG2, IgG3, IgG4
IgA1, IgA2
IgM1, IgM2
IgD
IgEd
28
Q

Allotypes

A

Minor allelic differences in the sequence of immunoglobulins between individuals, just as blood types or eye color differ.

Determined in mendelian fashion.

Occasionally an immunodeficient patients getting immunoglobulin treatments will make antibodies to someone else’s allotype.

29
Q

Idiotype

A

Each antibody has its unique combining region made up of CDR amino acids of its L and H chains

Antibodies can rarely be made to these sequences these are known as anti-idiotype.

In other words, an idiotype is an antibody’s unique combining site considered as an antigen.

30
Q

Allotypic exclusion

A

Only one H chain (maternal or paternal) and one L chain (kappa or lambda, either maternal or paternal) are synthesized in any one B cell. All other genes are silenced.

Each person can make two allotypes, but each B cell only makes one.

31
Q

Recombination

A

Changing the relative positions of two pieces of DNA.

Cell will choose one of its Vs, one D, and one J to make the VH domain gene.

First it brings one random D segment close to one J; the DNA is cut and the ends joined. It then repeats for V. The entire region from the assembled VDJ unit through the end of delta (IgD) constant region that is transcribed into RNA.

These primary RNA transcripts are alternatively processed using different poly-a sites and splicing to make VDJ-u and eventually VDJ-u and VDJ-delta messages.

Similar in light chain only there is V and J segments, no D and only one C domain gene.

This is done by RAG recombinases RAG-1 and RAG-2

32
Q

Somatic variation

A

The production of the V-D and D-J joints are sloppy. Exonucleases chew away a few nucleotides after DNA is cut before D-J or V to D are joined.

Then the cell adds a few nucleotieds with an enzyme called terminal deoxynucleotidyl transferase (tdt) which works at random.

Adds a great deal of variability

Two out of three times the N region, being a random length, will create a frame-shift mutation that is a nonsense mutation that will terminate transcription.

33
Q

Receptor editing

A

When a rearrangement is detected as faulty the RAG genes can try again. This is sometimes successful.

34
Q

Somatic hypermutation

A

The VDJ unit is hypermutable; each time a b cell divides after antigenic stimulation.

There is a good chance that one of the daughters will make a slightly different anitbody.

Selection is for the best fitting antibody which results in a gradual increase in anitbody-antigen affinity.

This is known as affinity maturation.

Activation-Induced Cytidine Deaminase (AID) converts random cytosines in CDR region to uracil. This newly made U:G mismatch gets excised and repaired w/ error prone DNA pols.

35
Q

Class switching

A

A single mature B cell starts making both IgM and IgD which can later switch to IgG, IgE, or IgA. In all cases, the L chain and the VH domain stays the same but the C region of the H chain changes.

36
Q

B Cell pro-proliferative cytokines

A

IL-2, IL-4, IL-5

37
Q

Cytokines that induce class switch to IgE

A

IL-4 and IL-5

38
Q

Cytokines that blocks class switch to IgE induced by IL-4

A

IFN-gamma

39
Q

Cytokine that induces class switch to IgG2a

A

IFN-gamma

40
Q

Cytokines that induces class switch to IgG1

A

IL-4

41
Q

Cytokine cause differentiation

A

IL-2, IL-4, IL-5, IFN-gamma, and TGF-Beta

42
Q

Important complement factors for clearance of immune complexes and apoptotic cells

A

C1, C2, C3, C4

43
Q

Complement factor important for opsoninizaiton

A

C3b

44
Q

Complement factor important for amplifying adaptive immunity

A

C3b

45
Q

Complement factor important for inflammation and T cell regulation

A

C3a and C5a

46
Q

Complement factor important for lysis

A

C5b, C6, C7, C8, C9

47
Q

C4b/C2a

A

C3 convertase in classical pathway

48
Q

C4b/C2a/C3b

A

C5 convertase in classical pathway.

49
Q

Bigger complement proteins that act as enzymes

A

C 4b, 2a, 3b, and 5b

50
Q

Smaller complement proteins that float off and recruit

A

C 4a, 2b, 3a, 5a

51
Q

Covalently binding tag complement proteins

A

C4b and C3b. Good if on bacteria and bad if on us.

52
Q

Classical pathway

A

C1q C1r C1s c4 and c2

53
Q

Mannose binding pathway

A

MBL, MASP-1, MASP-2

54
Q

Alternative pathway

A

Factor B, Factor D, and properdin

55
Q

Common to all pathways

A

C3

56
Q

Terminal lytic pathway

A

C5, C6, C7, C8, C9

57
Q

C3bBb

A

C3 convertase in alternative pathyway

58
Q

C3bBbC3b

A

C5 convertase in alternative pathway

59
Q

Properdin

A

Acts to stabilize the alternative pathway C3 convertase (C3bBb)

IHO Mike Rose (20 decks)

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