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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
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
Th17
Neutrophils
autoimmunity; inflammation
Tfh
B cells(autoantibodies)
CD8+ T Cells
MHC class 1
Directly kills infected cells
promotes activation and proliferation
CD4+ T Cells
MHC class 2
help B cells, macrophages, and other T cells
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
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