Humoral Immunity (Habal) Flashcards Preview

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Flashcards in Humoral Immunity (Habal) Deck (39):
1

The majority of intracellular pathogens are targeted by what kinds of cells?

T cells

2

How does the humoral response begin?

It's launched against extracellular pathogens.

3

What happens during the humoral response?

B cell activates against a specific antigen. It then undergoes clonal expansion & differentiation. Plasma cells secrete antibodies, which once produced have only a limited shelf-life (although they may persist longer). Memory B cells come along to provide long-lasting immunity.

4

Genes for heavy chains of antibodies come from which chromosome?

14

5

Genes for light chains of antibodies come from which chromosomes?

2-kappa & 22-lambda

6

What is the first Ig to be produced?

IgM

7

How do you go from IgM to IgG?

Get IgM first as it is genetically encoded in constant region. Post-rearrangement you get class switching - a loop forms, bringing the constant region for IgG or IgA closer to VDJ region, forming the class.

8

What are the effector mechanisms of the humoral response?

Agglutination (enhances phagocytosis), opsonization, neutralization (blocks toxin binding), inflammation, antibody-dependent cell-mediated cytotoxicity (NK cells), and activation of complement.

9

What are the 3 subsets of B cells?

Follicular, marginal zone, B-1

10

Describe follicular B cells.

T-dependent, isotype-switched (IgD & IgM), high-affinity antibodies; long-lived plasma cells. Found in spleen, other lymphoid organs. Respond to protein antigen and helper T cell.

11

Describe marginal zone B cells.

T-independent, mainly IgM; short-lived plasma cells. Found in white pulp of spleen. Respond to polysaccharides, lipids, nucleic acids.

12

Describe B1 B cells.

T-independent, mainly IgM; short-lived plasma cells. Found in mucosal tissues, peritoneal cavity. Respond to polysaccharides, lipids, nucleic acids.

13

What does class switching require?

T cell activation

14

What is the signal for class switching?

CD40 ligand

15

What do avidity and affinity of Ig refer to?

Avidity = strength of binding; affinity = specificty

16

What causes affinity maturation?

Continued exposure to antigens increases affinity over time, causing an increase in antibody specificity.

17

What are the secondary immune organs?

Lymph nodes, spleen

18

What is the main job of the red pulp of the spleen?

Filtration - RBC may be attached to opsonins that need to get cleared out.

19

What are people without spleens susceptible to?

Encapsulated organisms - no marginal zone B cells present to encounter them.

20

Where does class switching occur in the secondary immune organs?

Medulla

21

In the generation of antibody diversity, the heavy chain is rearranged first. With this rearrangement of BCR, you will have hypermutation. Define this, and explain its presence/absence in TCR.

Hypermutation - changes to the gene that enhance its specificity, but do not get transmitted to offspring. This is not seen in T cells.

22

B cells must be what in terms of T cells to class switch?

Be T-dependent.

23

What happens in Hyper IgM Syndrome?

Results from mutations affecting class switching (rare). Get a decrease in IgG, IgA, and IgE.

24

What would happen if you had a T Cell that doesn't express CD40L?

B cell is activated by T cell, but cannot class switch, so you'd only have an IgM response - but this decreases after about a week (not long-lasting). Thus you have a strong initial response that can knock out the organism, but not memory to fight it off at a strengthened initial attack should it come back - susceptible to repeated chronic infections.

25

If you have low levels of any specific Ig, what would you suspect to find in terms of levels of IgM?

They would be increased.

26

Describe IgM.

Pentamer when soluble , 1st Ig made by fetus and B cells, expressed as membrane-bound Ig, Fc receptor on phagocytes binds IgM (opsonization), present in colostrum & mother's milk to protect newborn, fixes complement. Higher avidity, lower affinity.

27

Describe IgG.

Monomer, major serum Ig, major Ig of secondary immune response, magor Ig in extravascular spaces, transported across placenta, fixes complement, opsonization. Longer lasting immune response because of memory and affinity maturation.

28

Which Ig gives an infant the immunity it needs during the 1st 6 months of its life?

IgG

29

Describe IgA.

Found in serum and body secretions - tears saliva, gastric, pulmonary (major secretory Ig); does not fix complement unless aggregated; present in colostrum & mother's milk (protects newborn); exists as dimer; gives infant some immunity.

30

Describe IgE.

Least common serum Ig (binds basophils & mast cells without needing Ag), allergic & hypersensitivity reactions, parasitic infections, does not fix complement; precipitates corsslinking after it has encountered antigen 2nd time after initial binding - get degranulation.

31

Describe IgD.

Found on membrane of mature B cells, present in very small amount in serum, does not bind complement, biological function not really understood.

32

How does T cell get activated?

When MHC presents (antigen) peptide to it.

33

What tells the B cell to start class switching?

CD40L on the antigen-specific T cell.

34

What stimulates the costimulatory signal?

CD28 on T cell binds to CD80/86/B7 of B cell.

35

What cytokine from which T cell is responsible for signaling clonal expansion of the B cell?

IL-4 from Th2

36

What cytokine from which T cell is responsible for signaling clonal differentiation of the B cell?

IL-5 from Th2

37

What triggers the process of B cell apoptosis and why?

FasL - kill the B cell if it interacts with something it's not supposed to, e.g. self-interaction.

38

Explain the classical complement pathway.

C1 binds to antibody complex, allowing it to cleave C2 & C4. C2b joins C4b to make C3 convertase, which either cleaves C3 or makes C35 convertase (in the presence of Properdin). Cleaved C3a creates an inflammatory response. Cleaved C3b opsonizes the antigen. C5 convertase cleaves C5. C5a creates an inflammatory response. C5b forms MAC when it reacts with C6-9. MAC makes a hole in cell membrane, leading to cell lysis.

39

Explain the alternative complement pathway.

Antigen reacts to C3b (always a little bit floating around). In presence of Factor B, Factor D, and Properdin, it forms a complex with these proteins to become C3 convertase. At this point it follows the same steps of the classical pathway, but either cleaving C3 or making C35 convertase (in the presence of Properdin). Cleaved C3a creates an inflammatory response. Cleaved C3b opsonizes the antigen. C5 convertase cleaves C5. C5a creates an inflammatory response. C5b forms MAC when it reacts with C6-9. MAC makes a hole in cell membrane, leading to cell lysis.