Adaptive immunity Flashcards
MHC1
- presents intracellular antigens to T cytotoxic cells
- all nucleated cells have the capacity to present intracellular antigens in the context of MHC1
steps of MHC1 presentation
- an intracellular antigen is broken into fragments by the cells proteasome
- the fragments are transported into the endoplasmic reticulum by a transporter protein
- the protein fragments associate with the MHC1 in the ER
- MHC1-antigen complexes make their way to the cell surface, where they are displayed for presentation to T cytotoxic cells
MHC2
- presents extracellular antigens to T helper cells
- only professional phagocytes have MHCII (macrophages, dendritic cells, and B cells)
steps of MHC2 presentation
- antigen presenting cell takes up extracellular antigens by phagocytes
- the endocytic vesicle fuses with a lysosome to make a phagolysosome, where the antigen is broken down. Vesicles carrying MHCII then fuse with the phagolysosome
- pieces of the antigen associate with MHCII
- the MHCII-antigen complex migrates to the cell surface to be displayed so that it can interact with T helper cells
what are the major professional antigen-presenting cells
- dendritic cells
- macrophages
- B lymphocytes
dendritic cell antigen presentation
presentation to naive T cells
macrophage antigen presentation
present to CD4 effector T cells
B lymphocyte antigen presentation
presentation to CD4 helper T cells
how do cytotoxic T lymphocytes kill
- when the TCR of a patrolling T cytotoxic cell binds to an MHC1 antigen complex it releases perforins and granzymes
- perforins form pores in the target cell
- granzymes enter through the pore and break down host cell proteins to induce apoptosis
subsets for helper T cells
- Th1
- Th2
- Th17
- Tfh
Th1
- targets and secretes cytokines to activate macrophages to M1 to make it pro-inflammatory
- defend against intracellular pathogens
- role in autoimmunity and chronic inflammation
Th2
- targets and activates eosinophils
- pushes macrophages to M2 (dampens inflammation)
- defends against helminths
- role in allergies
Th17
- targets, recruits, and activates neutrophils
- defends against extracellular bacteria and fungi
- roles in autoimmunity and inflammation
Tfh
- targets B cells
- stimulates antibody production
- defends against extracellular pathogens
- role in autoimmunity (autoantibodies)
mycobacteria
inhibit phagolysosome production
herpes simplex virus (HSV)
inhibits antigen presentation; interferes with transport of pieces of antigen into the ER for antigen presentation
cytomegalovirus (CMV)
inhibits antigen presentation; stops proteasomal activity and removes class 1 MHC molecules from the ER
Epstein-Barr virus (EBV)
inhibits antigen presentation; inhibits proteasomal activity; inhibits macrophage and dendritic cell activation
Pox virus
inhibits effector cell activation; produce soluble cytokine receptors
IgG
- monomer
- most abundant
- crosses placenta *key for babies
IgA
- can be a monomer or dimer
- second most abundant
- main antibody in milk, resistant to destruction by stomach acid
IgM
- monomer or pentamer
- third most abundant
- made FIRST in infection; large structure limits where it migrates
IgE
- monomer
- rare
- fights parasites; mediates allergic responses
IgD
- monomer
- rare
- bound to B cells; poorly understood
how antibodies eliminate invaders
- neutralization of antigens
- activate complement cascade
- increase phagocytosis
primary response lag after immunization
5-10 days
secondary response lag after immunization
1-3 days
primary response peak response
smaller
secondary response peak response
larger
primary response antibody isotype
IgM>IgG
secondary response antibody isotype
relative increase in IgG and under certain situations in IgA or IgE
primary response antibody affinity
lower average affinity, more variable
secondary response antibody infinity
higher average affinity (affinity maturation)
VDJ recombination
creates a large diversity of antibodies and receptors
CD8 T cells
- cytotoxic cells
- recognize MHC I antigens presented by cells that have intracellular microbes
CD4 T cells
- helper cells
- recognize extracellular antigens that have been phagocytized by APC and presented on a MHC II complex
humoral response
- controlled by B cells
- B cell receptors bind to antigens epitope
- antigen enters cell by endocytosis and then is displayed on MHC II
- MHC II antigen complex on B cell is then bound by T helper cell
- cytokines are released upon proper T helper cell binding (T-dependant)
- once activated B cell proliferates and differentiates into plasma cells or B memory cells
plasma cells
release antibodies
B memory cells
save information about the antigen
IgM>IgG
early infection
IgM<IgG
late infection
naturally acquired active immunity
immunity gained from a previous infection
naturally acquired passive immunity
antibodies pass from the placenta to the fetus
artificially acquired active immunity
vaccination triggers immune response
artificially acquired passive immunity
given antibodies against a toxins; wont mount own response
