Lecture # 20 B Cell Activation and Effector Function Flashcards Preview

Medical Immunology Bios 443/843 > Lecture # 20 B Cell Activation and Effector Function > Flashcards

Flashcards in Lecture # 20 B Cell Activation and Effector Function Deck (31):

Why do CD8 cells require more co-stimulation?

Because they are destructive



Receptor on the surface of T cells, binds to ICAM-1 on an infected cell or APC


Immunological synapse

The point of contact between a CD8+ cell and its APC; outer ring adhesion molecules; inner ring: signaling molecules. granules behind the synapse align with cytoskeleton once binding occurs


What are the two compounds that CD8 cell produce to induce apoptosis?

Perforin and Granzymes



Pore forming protein-aids in delivering contents of granules into the target cells



serine proteases-activate apoptosis once inside the target cell; activate caspases--GrB cleaves and activates caspase 3; acts on mitochondrial proteins and eventually activates CAD that fragments DNA and leads to cell death.



a part of the perforin/granzyme complex; may play an important role in protecting the CD8 cell from damage.


What dictates follicular B Cell location in the LN?

The expression of CXCL13 and CXCR5.


How many signals do B cells require for full activation?

Two signals: Signal #1 T microbial antigen binding to BCR; #2 PRR engagement or complement by R (PRR engagement is T independent) T dependent require interaction with CD40L


Thymus Independent Responses type 1

TI-1; some TI-1 antigens are called B cell mitogens; LPS can induce polyclonal activation, non specific antibodies at high concentrations-activates TLR4


Thymus Independent Responses type 2

TI-2; Ags are characterized by having multiple identical epitopes: polysaccharides; B1 cells and marginal zone B cells important for TI-2 responses;Usually IgM produced but some cases switching to IgG


What is signal # 2 for T-dependent Antigens?

Signal 2 is provided by CD40:CD40L and cytokines



Present on lymphocytes. Is up-regulated after CCR7 is down-regulated;purpose is to aid in migration to the follicle; is a receptor for CXCL13 (chemokine)



proliferating cell marker (centroblasts); present on actively proliferating B cells


FDC (anti-CD3)

Help to retain Ag in the GC secretes CXC13;


What happens as B-Cells move through GCs?

they undergo somatic hypermutation, affinity maturation and isotype switching


IgM function

Complement activation


IgG function

opsonization, phagocytosis, complement activation, neonatal immunity


IgE, IgG4 function

Immunity against helminths, mast cell degranulation (immediate hypersensitivity); Th2 cell induced


IgA function

mucosal immunity (transport of IgA through epithelia)


Receptors on B cell (for T cell interaction)

(B7-1 and B7-2); CD40; MHC II or I


Receptors on T cell (for B cell interaction)

(CD28 reacts with B7-1/2) CD40L


Class switching

Activated by cytokines inducing transcription of switch region upstream of C region; lies in intron b/w J region and C u and upstream of all other C genes; Th1-> IgG1, IgG3, while Th2 -> IgG4 and IgE


Process of class switching

Occurs after B cells encounter Ag; RNA-DNA hybrids for in the switch region; AID (activation induced cytidine deaminase) converts cytidine to uracil; UNG removes the uracil leaving abasic sites APE1 cleaves abasic sites leaving a nick in the DNA, ds breaks are repaired by normal ds break repair mechanisms.


Somatic Hypermutation

mechanism to induce point mutation in the V regions of existing BCR; mutations occur 1000x; AID also plays a huge role; result is a multitude of B cells with different affinity receptors. Those BCRs that bind with high affinity receive survival signals. (selection occurs by follicular DCs)


Where do the point mutations in somatic hypermutation accumulate?

Point mutations accumulate in the BCRs of the VH and VL chains.


Which Co-receptor is necessary for the Th activation?

CD28 not CTLA-4 binds to B7-1/B7-2 for activation. CTLA-4 binds to B7-1/2 with higher affinity and tells the cell to stop proliferating and limits the binding of CD28 and B7-1/2


CTL binding and destruction of target cells depends on:

antigen presentation on the surface of the target cells.


Antigen binds to T cells first and divide in response to IL-2 and then differentiate into effector helper or cytotoxic cells (T/F)

T (CD8 and CD4 proliferate in repsonse to IL-2) and then other cytokines cause differentiation


Only viral or bacterial infected cells are susceptible to CTL-mediated apoptosis (T/F)

T (CTL-mediated apoptosis only occurs on virally infected cells; non-infected cells are spared)


Conventional DCs secrete high levels of IFN-b in response to viral infection (T/F)

F CDCs secrete IL-12; uptake antigen; migrate from sites from infection to lymph nodes; involved in presentation

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