Adaptive Immunity

Antigenicity

the key can fit into the lock

Immunogenicity

the key can make the lock turn and open the door

MHC Class I

Found on all nucleated cells

Presents peptides from inside the cell (self or viral proteins)

Recognized by CD8⁺ cytotoxic T cells

Function: lets T cells detect virus-infected or abnormal cells

MHC Class II

Found mainly on antigenpresenting cells (APCs) such as macrophages, dendritic cells, and B cells(porfessional phagocytes)

Presents peptides from engulfed extracellular microbes

Recognized by CD4⁺ helper T cells

Function: helps activate immune responses against extracellular pathogens

MHCI: Presenting Intracellular Antigens to T Cytotoxic Cells

All nucleated cells have the capacity to present intracellular antigens in the context of MHCI(protosome)

MHCII: Presenting Extracellular Antigens to T Helper Cells

Only professional phagocytes have MHCII (macrophages, dendritic cells, and B cells)(phagolysosome)

epitope

specific part of a antigen

CD4+ Helper T cells

“Help” Both Branches of Adaptive Immunity

Effector T cells

Th1

Th2

Th17

Tfh

Th1

macrophages

inflammation

Th2

eosinophils

allergy and allegries

Th17

Neutrophils

autoimmunity; inflammation

Tfh

B cells(autoantibodies)

CD8+ T Cells

MHC class 1

Directly kills infected cells

cytokines promotes activation and proliferation

CD4+ T Cells

MHC class 2

help B cells, macrophages, and other T cells

cytokines guides Th subset formation

Cytotoxic T Lymphocyte (CTL or CD8+ or killer T cell)

a cell is infected with a virus or if it is cancerous, interferons are released

What happens when interferons are released

Recruits activated T cytotoxic cells to the area

Enhances MHC I production inside host cells

Puts the immune system on high alert

Cell-mediated response CD8+ T killer cells/CTLs

when TCR of a patrolling T cytotoxic cell binds to an MHC I– antigen complex it releases perforins and granzymes

perforins

Forms pores in the target cell

granzymes

Enter through the pore

Break down host cell proteins

Induce apoptosis

Antibody Structure

tips of the molecule are the antigen-binding sites

2 heavy chains 2 light chains Held together by covalent bonds

Antibody Structure and Isotypes

IgG

IgA

IgM

IgE

IgG

monomer

must abundant

good at everything

lasts the longest

crosses placenta and give babies antibodies

IgA

Monomer or dimer

antibodie in milk

resistant to sotmach acid

IgM

Monomer or pentameter

activates comploment system

first antibody in blood in infection

IgE

Monomer

parasites and allergic responses

What are antigens dependent on

T helpers to fully activate B cells

How antibodies eliminate invaders:

neutralization

activation

increase

Neutralize antigens

Antibodies block toxins or antigens from binding to host cells

Activate complement

Cytolysis Opsonization Inflammation

Increase phagocytosis

Precipitation Agglutination Opsonization

precipitation

making a solid from dissolved stuff

agglutination

clumping things that were already solid

nAbs

• Neutralizing antibodies

mAbs

• Monoclonal antibodies

Fab

• Fragment antigen-binding

scFv antibodies

Chimera of variable heavy and variable light chains

Primary Antigen Exposure

IgM and IgG peak are same

Secondary Antigen Exposure

IgG has a giant peak over IgM

antigen

substance that the body's immune system recognizes as foreign and that can trigger an immune response

Increasing immunogenicity

small molecules then lipids then polysaccharides then protein

Migration of macrophages

free floating and in brain, liver, lung ,spleen

Migration of macrophages Brain

Microglial cells

Migration of macrophages Liver

Kupffer cells

Migration of macrophages Lung

Alveolar macrophages

Migration of macrophages Spleen

Sinusoidal macrophages

Capture, transport and presentation of protein antigens by dendritic cells

Dendritic cells that are primarily located in the epidermis are called Langerhans cells

Naturally acquired active immunity

Immunity from a previous infection

Naturally acquired passive immunity

Antibodies pass across the placenta

Artificially acquired active immunity

Vaccination triggers immune response

Artificially acquired passive immunity

Antivenom neutralizes toxins

Humoral immunity

b lymphocytes

block infections and elimate extracellular microbes

Cell-mediated immunity

Helper T lymphocytes

elimination of phagocytosed microbes

Cytotoxic T lymphocyte

Kill infected cells and eliminate reservoirs of infection

Where do T cells go

Thymus

Where do B cells go

bone marrow

T cell activation

antigen specific signals

costimulatory molecules

cytokine

Cell-mediated immunity

phagocyte with ingested microbes in vesicles

infected cell with microbial antigens in cytoplasm

phagocyte with ingested microbes in vesicles

cd4+

macrophage activation killing of ingested microbes and inflamtion of killing of microbes

Th1 and Th17

infected cell with microbial antigens in cytoplasm

CD8+

killing of infected cells

Can microbes evade cell-mediated immunity

yes by inhibition of macrophage activation or antigen presentation

or by block cytokine activation of effector cells

T-independent antigens

multiple binding cites for B cells

What happens to Activated B cells

proliferate and differentiate into plasma cells and memory cells

Function: Release antibodies

High diversity of immunoglobulins and Tcell receptors

V(D)J ordered recombination of gene segments

Variable • Diversity • Joining