Humoral Immune Response Flashcards by Eric Pohlen

Components of mature naive B cell

BCR: IgM, IgD, Ig a & Igβ

Co-BCR: CD19, CD81 & CR2 (CD21)

HLA-Class II

CD40

CD20

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Two Types of B-2 cells

Follicular B cells are re-circulating B cells: Majority

Marginal B cells reside in the spleen: blood-borne polysaccharide Ags

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What signal allows for migration to the Primary Follicle

CXCR5

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First Signal Activation

via mIgs

Must cross link 2 or more BCR

signaling occurs through Igα& Igβcytoplasmic tails

phosphorylation of Syk-B
activate PLCy
leads to inositol triphosphate and DAG
activate Ca2+ dependent enzymes and PKC

Also Activation of RAS and RAC lead to ERK and JNK

All three pathways promote Myc, NFAT, NFkB, and AP-1 which increase
protein synthesis

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First signal helping activation signals

Ag bound with C3d binds CR2 and enhances signal 1000 fold. Occurs through: Igα& Igβ, CR2 & CD19 cytoplasmic tails (BCR co-receptor complex*)

also can be TLR signaling

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Outcomes of First signal

Increased survival and proliferation
Interaction with helper T cells (increased B7 expression)
Responsiveness to cytokines
Migration from follicle to T cell area (expression of CCR7)
Secretion of IgM

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what are the two types of Second Signals

T independent signal- would be the mitogen
T dependent antigen would be the T helper cell and the CD40/CD40L interaction

Both signals cause the B cell to Proliferate and expand

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Once activated by T helper cells B cells will begin to?

Change their chemokine receptor expression (class switch) and affinity maturation

Successful re-arrangements are selected/supported by TFH and follicular dendritic cells

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What two things do cytokines released by Th cells promote

induce H chain class switching

- Augument B cell differentiation and proliferation

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Cytokine IL-4 causes activated Isotype switching in B cells to?

IgE

Immunity against Helminths and Mast cell degranulation

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Cytokine TGF-beta, APRIL, BAFF causes activated Isotype switching in B cells to?

IgA

Mucosal Immunity

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Cytokine IFN-y causes activated Isotype switching in B cells to?

IgG?

Opsonization of phagocytosis and complement activation

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Switch Recombination occurs in what region of DNA and by what type of antigen

CD40: CD40L ligation and cytokines in T dependant AG binding (protein)

Occurs in a downstream C region, intervening DNA is deleted

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Affinity Maturation

Introduction of Point Mutations in the Variable areas of Ig genes

AID converts C’s to U’s

UNG creates the abasic cites

Ape 1 Endonuclease generates nick ( double strand breaks in DNA)

Idea of Somatic Hypermutation,

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Where do the majority of Mutations occur in Somatic Hypermutation

Heavy chain and Light chain V regions,

Mutations mainly occur in secondary and Teritary Antibodies

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Characteristics of T follicular Helpers

CD4+ and low levels of CD25 expression

Have ICOS/ICOS-L essential for germinal center reaction

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What do T follicular helper cells secrete?

IL-21 to facilitate differentiation to plasma blasts

also provide IFN-y and IL-4 cytokine for switching

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What is the selection checkpoint?

Where T Follicular Helper cells and Follicular Dendritic Cells choose the B cell with the highest Affinity to the presented antigen for its necessary survival

Rest of cells Apoptosis

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Plasma Cell components?

Terminally differentiated effector B cell

Decrease in CD19 and CD20 expression,

Increase in CD27 cell marker

only secrets its class dependent Antibody

Expansion of ER in Cytoplasm

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What is the effector of the Humoral Immunity

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Antibodies

What is the type of B cells that are T-Independant

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B-1 cells respond to T- independent responses (non-protein) Ag in mucosal tissues

Marginal zone B cells (B-2) in spleen recognize blood-borne polysaccharides.

What do T-independent cells secrete

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IgM

Considered short lived plasma cells

Memory B cell components

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Survive long time without AG

Express high levels of Bcl-2 (anti-apoptotic protein)

surface markers: CD27 and CD45R(O)

Secretory class Ig dependant

Capable of mounting rapid response to similar Ag: Secondary immune mresponse

Antibody feedback

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Control mechanism triggered by IgG and when there are too many antibodies for an ending immune response

ITIM - activates SHIP which blocks B cell receptor signaling

what is the effector region of of an antibody and how is it triggered

Fc Region is the effector function but it is triggered by the binding of Ag to Fab(V) region

Aspects of the Primary Response

usually 5-10 days peak is smaller usually more IgM vs IgG Lower affinity

Aspects of the Secondary Response

Usually 1-3 days peak is larger More IgG and even IgA or IgE Higher average Affinity

Antibody Effector functions

Neutralize microbes and toxins Opsonization and phagocytosis of microbes Antibody dependent cellular cytotoxicity Complement activation - inflammation - lysis of microbes - Phagocytosis of microbes with complement fragments

What binds to Fc and what is Fc's two main functions

FcR Deliver antibody to inaccesible anatomical sites link bound antigen to molecules/cells that effect destruction

FC receptor FcyRI (CD64)

High affinity for IgG On -Macrophages, neutrophils, eosinophils Function: Phagocytosis

FcyRIIA (CD32)

low affinity Macrophages and Neutrophils and eosinophils Phagocytosis, and cell activation

FcyRIIB (CD32b)

Low affinity B lymphocytes,DC, mast cells, and neutrophils Feedback inhibition of B cells attenuation of inflammation

FcyRIIIA (CD16)

Low affinity NK cells Antibody dependant cellular cytotoxicity

FceRI

High Affinity mast cells and basophils and eosinophils Activation/degranulation of mast cells and basophils

Neutralization via Ntibodies

Any Ab class can do this Blocks penetration of microbe through epithelial barrier Blocks binding of microbe and infection of cells Blocks binding of toxin to cellular receptor

Waste Management

Clearance of immne complexes CR1 on erythrocytes bind to C3b or C4b on IC floating through the blood Take to spleen or liver to drop off IC IC gets phagocytosed by local macrophage

ADCC anti viral state

NK binds to CD16/ FcR receptor on IgG that locates a surface antigen on host cell NK kills the cell

IVIG

treats autoimmune/ inflammatory disesses Ig engages the inhibitory FcR on B cells and DC

Natural Antibodies

IgM and some IgG Produced by B-1 and marginal zone B cells reacts with alloantigens (ABO blood type)

IgE mediated reactions

Binds FceR on Eosinophils and mast cells and cause them to degranulate to kill helminth

Mother provides what types of immunity for fetus and babies

Physical barrier for fetus IgG during pregnancy IgA through secreted breast milk

What receptor does IgG travel through in the placenta

FcRn due to the low pH causes the tight binding to prevent lysosome destruction

Why are babies at risk for disease after birth

IgG and IgA are just starting to be synthesized IgM has started only a little bit

Passive Immunity

given antibodies Prevent disease after known exposure protect immunosuppressed patients get rid of ongoing symptoms Prevent the cause of the disease ie snake bite mother giving antibodies to child

Active Immunization

Delayed but more permanent Produces immunological memory ie natural exposure vaccines

Criteria for an effective vaccine

safe provide protection cost effective establish long term immunity

Problems with vaccines

Clinically important epitopes may not be intact in vaccine• Individual genetics may effect efficacy• Some individuals may be genetically predisposed to adverse events • Often work poorly in very young infants or the elderly• Many do not induce CMI; Ab may not be sufficient• Allergies to vaccine components

Types of evasions of the Humoral immunity

Antigenic Variations Inhibition of complement activation Blocking by Hyaluronic Acid capsule

Humoral Immune Response Flashcards

(48 cards)