Term
| To communicate antigen interaction into the interior of a B cell, Ig-alpha and Ig-beta ITAMS associate with what tyrosine kinases? |
|
Definition
| Blk, Fyn, and Lyn. (once phosphorylated, Syk binds to Ig-alpha and Ig-beta tails, initiates intracellular signaling pathway). |
|
|
Term
| What additional signaling is needed to activate a naive B cell? (co-receptor of what 3 proteins) |
|
Definition
B cell co-receptor of 3 proteins:
CD19 (signaling chain)
CD21 or CR2 (brings pathogen and B cell together)
CD81 (unknown function) |
|
|
Term
| What are thymus-independent antigens? |
|
Definition
| A short list of antigens that provide enough signal potential to stimulate naive B cells to produce antibody. |
|
|
Term
| How do T1 thymus independent antigens stimulate B cells? |
|
Definition
| Engage multiple receptors (e.g. Toll like receptors) |
|
|
Term
| How do T2 thymus independent antigens stimulate B cells? |
|
Definition
Cross-link B cell receptors and co-receptors extensively, need for additional signals is overriden.
Composed of repeated epitopes on polymeric antigens. |
|
|
Term
| How are naive B cells attracted to a lymph node? |
|
Definition
| CCL19 and CCL21 (same as T cells) |
|
|
Term
| What are 3 sequenced required signals for naive B cell stimulation? |
|
Definition
1. BCR binds soluble antigen
2. CD40 receptor binds CD40 ligands on TH2 cell, inducing cytokine receptors on B cell
3. Cytokine receptors bind IL-4, IL-5, and/or IL-6 from the cell. |
|
|
Term
| What happens to cognate T-B pairs? (2 things) |
|
Definition
1. Migrate to medullary chords, undergo mitosis, secrete some antibodies into lymph node
2. Migrate to B cell area follicles to form germinal center |
|
|
Term
|
Definition
| Complex of a pathogen or antigen with complement retained on surface of a follicular dendritic cell. |
|
|
Term
|
Definition
| Large, metabolically active accumulation of dividing B cells (forming high affinity antibodies--dark zone of germinal center) |
|
|
Term
| What is a germinal center? |
|
Definition
| Contains rapidly dividing T and B cells |
|
|
Term
|
Definition
| Rise from centroblasts, divide more slowly and express surface immunoglobulins, now mutated and switched in isotype (light zone). |
|
|
Term
| What cytokines from TH2 cells influence isotype switching of centroblasts? |
|
Definition
|
|
Term
| True or False: TH2 derived IL-4 favors memory B cell formation. |
|
Definition
| True (IL-10 favors plasma cell formation) |
|
|
Term
| Where is IgM primarily located? What does it do? |
|
Definition
| In the blood; its a pentamer that activates the complement cascade |
|
|
Term
| Where is IgA? What does it do? (monomeric) |
|
Definition
| It's in the blood, but can get into tissues. It neutralizes, fixates complement, and opsonizes. |
|
|
Term
| Where is IgA? What does it do? (dimeric) |
|
Definition
| Protects surface of mucosal epithelia. It prevents attachment, colonization of mucosal epithelium, facilitates expulsion of pathogens in feces, sputum, tears, and other secretions. |
|
|
Term
| Where is IgG? What does it do? |
|
Definition
| It is prevalent in serum, and is transported into tissues. It neutralizes pathogen in the blood, also complement fixation and opsonization. |
|
|
Term
| How is IgG delivered to tissue? |
|
Definition
| FcRn-mediated transcytosis to interstitial spaces. |
|
|
Term
| Which antibodies are present passively in neonates? |
|
Definition
| IgG (placenta) and IgA (dimer--breast milk) |
|
|
Term
| True or False: Most vaccine strategies elicit neutralization antibodies that prevent infection. |
|
Definition
|
|
Term
| What helps erythrocytes clear antigen/antibody complexes from blood? |
|
Definition
| CR1 (binds C3b on the complex) |
|
|
Term
| How do NK cells use antibody to identify and assess cells? |
|
Definition
| Use CD16; when they encounter cells with igG antibody, they rapidly kill the target cell. |
|
|
Term
| Describe complement fixation by antibody. |
|
Definition
| IgM pentamer or 2 IgG molecule bind antigen, expose binding sites for C1q component of C1. Activated C1 cleaves C2 and C4, and C2a and C4b fragments form classical C3 convertase on pathogen surface. Conversion of C3 to C3b leads to attachment of C3b on pathogen surface and recruitment of effector functions. |
|
|
