CH 8: adaptive immunity

adaptive immunity

specific

memory

work together w/inflammation

recog foreign or nonself substance

adaptive immunity produces

lymphocyte: T/B cell

antibodies: immunoglobulin (Ig)

clonal diversity

primary lymphoid organ

mature B/T cells

migrate to secondary lymphoid organ

occur in fetus

clonal selection

antigen processed to immune cell by antigen-presenting cell (APC)

cellular interaction of T helper cell and APC

effector ( Th, plasma, Tc cell) and memory cell

T cell

thymus

B cell

bone marrow

humoral immunity

B cell, circulating antibodies

direct inactivation of microorganisms or activation inflammatory mediators

protect against bacteria, viruses

cellular immunity

T cell

protect against viruses and cancer

active immunity

body make own antibodies

from infection or vaccine (Long-lasting)

passive immunity

antibodies transfer from another source

temporary

antigen

react w/antibodies or receptor on B/T cell

trigger immune response

protein

steps:

1. bind

2. processing

3. presentation (MHC)

immunogenic antigen

antigen can trigger an immune response

epitope

antigen binding site

recognize by antibody

paratope

antibody binding site

matching on antibody

haptens

small molecular weight antigen

cant trigger immune response alone, but bound to carrier protein

tolerance

recognize ourself as not foreign

central/peripheral

central tolerance

lymphocyte w/receptor against self antigen are eliminated

peripheral tolerance

prevent recognition by lymphocytes and antibodies

B lymphocyte

present antigen to Th, facilitate humoral immune response

Macrophages

present antigen to memory Th, rapid response to antigen (secondary immune response)

dendritic cell

process antigen from site of inflammation to T cell rich area of lymph node

antigen processing

exogenous and endogenous antigen linked with MHC molecule

Class I MHC

Class II MHC

class I MHC

present endogenous antigen (inside)

class II MHC

prefer exogenous antigen (outside)

molecules that recognize antigen

circulating antibody

antigen receptor B cell (BCR)

antigen receptor T lymphocyte (TCR)

B cell clonal selection

1. Antigen processed & presented on MHC II 

2. Th2 cell activates B cell 

3. B cell becomes: 

4. Plasma cell (antibody factory) 

5. Memory B cell

class switch

isotype

1. Requires CD40–CD40L interaction 

2. IgM → IgG, IgA, IgE 

3. T-independent antigens cannot class switch

immunoglobulin

antibody

IgG

IgA

IgM

IgE

IgD

IgG

transported across placenta

protective against infection

most abundant

IgA

secretion (saliva, breast milk, mucus)

mucosal antibody

dominant immunoglobulin

IgM

largest immunoglobulins

first antibody produced during response to antigen

fetal

IgD

concentration low in blood

function limited

IgE

least concentrated

acts as mediator of many common allergic responses

defend against parasite

antigen-binding fragment (Fab)

recognition site for antigenic determinants, 2 identical fragments

crystalline fragments (Fc)

biologic function

activate complement/opsonization

polypeptide chain (four)

two light change, two heavy chain held with disulfide bond

heavy chain determine antibody type

antibody function: direct

neutralization: inactivate or block antigen to receptor

agglutination: clump insoluble

precipitation: soluble antigen into insoluble precipitate

antibody function: indirect

inflammation

phagocytosis

complement

antibody titer

level of circulating antibodies

primary immune response

initial exposure

latent period or lag phase

prime

IgM then IgG

secondary immune response

anamnestic

large amount antibody

memory cell

more IgG

T cell activation

cellular immune response

bind antigen

direct killing foreign/abnormal cell

Th1

help dev cell-mediated immunity

activate macrophages/Tc cell

Th2

help dev humoral immunity

activate B cell

Th17

help inflammatory response

Tc lymphocyte

destroy cancel or virus infected cell

perforin

penetrate, polymerizes, form pore in target cell plasma membrane

granzyme

enter cell through perforin-lined pores, activate cellular enzyme (caspases)

direct receptor interaction

signal target cell to undergo apoptosis

NK cell

complement to Tc cell mechanisms

kill abnormal cell w/o MHC class I

attach to IgG

chronic inflammation

T cell produce cytokines

T reg lymphocyte

suppress immune responses

provide peripheral tolerance

control/limit immune response to protect hosts own tissue against autoimmune reaction

fetal/neonatal immune function

immature immune system

receive IgG from mom

only produce IgM

aging immune function

decrease T cell activity, production specific antibodies, circulating memory B cell, autoantibodies

antibodies

y shaped protein

neutralization, opsonization, complement activation

t-lymphocte

• Helper (CD4): Coordinate response

• Cytotoxic (CD8): Kill infected cells

• Regulatory: Suppress immune response

• Memory: Long-term immunity