Specific Acquired Immunity - Diebel Flashcards
T Cell Function
Survey the surfaces of cell’s looking for ones that have been infected
or that are dangerously changed/mutated
-CELL MEDIATED IMMUNITY
B Cell Function
Fully differentiated=Plasma cell
Protects extracellular spaces of body by RELEASING ANTIBODIES into fluids
- Don’t require recognition of MHC or presentation
- HUMORAL immunity
IgG functional properties
- Most abundant
- 6 IgG’s cooperate to activate COMPLEMENT –> inflammation
- some can lyse bacterium by making holes in memebrane
- ONLY Ig that passes the placenta from mother to fetus
IgM
- VERY good at activating complement
- 1st antibody type to appear in blood after exposure to a new antigen (then replaced by IgG
IgD
-inserted into B cell membranes as their antigen receptor.
IgA
- Ig in secretions like saliva, tears, genitourinary, and intestinal fluids, milk
- associated with SECRETORY COMPONENT, which it acquires from epithelial cells during the process of being secreted.
-Secretory component makes it resistant to digestive enzymes
IgE
- attaches to MAST CELLS
- When IgE finds antigen it causes mast cell to make –> prostaglandins, leukotriends, and cytokines
- —> release granules that contain histamine
- -Produce allergy symptoms
- -Real role of IgE is in resistance to parasites
MHC I
What cells are they on?
how do they work?
What cell do they stimulate?
On ALL cells except RBC
-Antigen synthesized WITHIN the cell.
Infected with a virus –> Cell breaks down virus and displays it on MHC I
-CD8+ killer T cells see the display
MHC II
What cells are they on?
how do they work?
What cell do they stimulate?
- on monocytes/macs, DC, B cells, and epithelial cells of thymus
- antigens are products of PHAGOCYTOSIS
- APC’s bring antigen to T or B cells and activate them?
Th1 helper T cell:
- T cell migrates to site of invasion
- re-stimulated by local APCs and release lymphockines
- these attract and activate monocytes and macrophages
- ==Intense inflammation
Cytotoxic/Killer T cells:
CD8+ response:
Kills cells they recognize as having abnormal molecules being displayed on MHC I
What do all T cells express?
CD3 and have T cell receptors
Th17 Helper T cells
- cause focused inflammation
- MORE powerful than Th1
Th2 helper T cell
- Stimulate macs to become M2s.
- wall off pathogens and promote healing
- very important in PARASITE immunity
Tfh (follicular)
- stimulated by antigen
- migrate from T cell area of lymph nodes into B cell follicles
- BOOM! help B cells get activated
- Also provide some instructions about what Ig the B cell should make.
Treg (regulatory)
Make IL-10 cytokine that SUPPRESSES the activation/function of Th1, Th17, Th2 cells
-Keeps the immune system in check
What cells have CD4+ molecular marker?
Th1, Th2, Th17, Tfh, Treg
What molecular markers do B cells have?
Igs,
CD40
CD79a
CD79b
Activation of AlphaBeta T cells?
2 steps!
Signal 1. TcR recognition of HLA bound antigen
-CD4+ + MHC II or CD8+ + MHC I
Signal 2: B7-1 (CD80) or B7-2 (CD86) on APC binds to T cell surface protein CD28
Other costim:
- CD2 on T cell binds to CD58
- LFA-1 on T cell binds ICAM
- cytokine signals
General activators of T cells (cytokines)
IL-2 (autocrine)
IL-15
Th0 —> Th1 cytokine stimulus?
IL-12 and IFN-gamma
Th0 —-> Th2 cytokine stimulus?
IL-4
Cytokines that down regulate Th1?
Th2?
IL-10 down regs Th1
TGF-beta down regs Th1 and Th2
Killer T cell– Kill by FAS
T cell expressing FAS ligand binds to FAS protein on target cell
–> induces caspase activation and apoptosis
Killer T cell– Kill by secreting Toxic agents
- Secrete TNF that can induce apoptosis.
- Secrete Perforin: pore forming protein
- Granzymes: induce apoptosis
What pathogens are antibodies important for?
Extracellular!
-Staphlococcus, Streptococcus, Hemophilus
X linked agammaglobulinemia (B)
Absence of B lymphocytes
CD40 ligand deficiency (B)
Failure of Ig class switching
Activation-induced Cytidine Deaminase Defiency (B)
Failure of Ig class switching
Common Variable Immunodeficiency (B)
Failure to produce antibodies against particular antigens
Omenn Sydnrome (B & T )
VDJ recombination failure.
Can’t produce BCRs or TCRs
X-linked severe combined iummnodeficiency (T)
Failure to produce mature T lymphocytes
DiGeorge Syndrome (T)
Failure of thymus to develop correctly
Hemophagocytic lymphohistiocytosis (T)
Failure of CD8+ T cells and NK cells to produce and/or release lytic granules
IPEX (T)
Failure of peripheral tolerance due to defective regulatory T cells
