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FA random immune

QuestionAnswer
Found in lymph node follicle B cells
Found in medullary cords of lymph nodes lymphocytes and plasma cells
found in medullary sinuses of lymph nodes reticular cells and macrophages
found in the paracortex of lymph nodes T cells
Where are T cells found in the spleen? Periarterial lymphatic sheath (PALS)/white pulp
Where are B cells found in the spleen? Follicles/white pulp
decreased IgM leads to decreased complement activation leads to decreased C3b opsonization splenic dysfunction
increased susceptibility to encapsulated organisms (S SHiN) splenic dysfunction
Found in patients after a splenectomy Howell-Jolly bodies, target cells, thrombocytosis
Where do Positive and negative selection occur? at the corticomedullary junction
positive selection MHC restriction
negative selection nonreactive to self
binds TCR and CD8 MHC 1
HLA-A, HLA-B, HLA-C MHC 1
binds TCR and CD4 MHC 2
HLA-DR, HLA-DP, HLA-DQ MHC 2
where is MHC 1 expressed? all nucleated cells, NOT RBCs
where is MHC 2 expressed? only on APCs
enhances activity of NK cells IL-12 IFNbeta IFNalpha
When are NK cells induced to kill when exposed to a nonspecific activation signal on target cell OR absence of class I MHC on target cell surface
How do NK cells induce apoptosis of virally infeceted and tumor cells? Using perforin and granzymes
costimulatory signal of Th cell activation B7 and CD28
constimulatory signal of Tc cell activation IL2 (from Th) to IL2 receptor
signal one of B cell class switching IL-4,5,6
signal 2 of B cell class switching CD40 receptor (B cell) CD40 ligand (Th cell)
Activates macrophage and CD8+ T cell Th1
regulates cell mediated response Th1
regulates humoral response Th2
helps B cells make ab (IgE>IgG) Th2
Determines Ig isotyple Fc
enzyme for random recombination of VJ (light chain) or V(D)J (heavy chain) terminal deoxynuleotidyl transferase adds nucleotides to DNA
initiates the alternative complement pathway Microbial surfaces (endotoxin)
initiates the classic complement pathway Antigen-antibody complexes
membrane attack complex C5b,6,7,8,9
Decay-accelerating factor (DAF) CD55, CD59
The 2 primary opsonins in bacterial defense C3b and IgG
system of proteins that interact to play a role in humoral immunity and inflammation complement
C3b opsonization
C3a, C5a anaphylaxis
C5a neutropil chemotaxis
Deficiency of C1 esterase inhibitor hereditary angiodemia because of increased bradykinin
Severe recurrent pyogenic sinus and respiratory tract infections (strep pneumo, H flu) C3 deficiency
increased susceptibility to type III hypersensitivity reactions (glomerulonephritis) C3 deficiency
Neisseria bacteremia C5-C8 deficiency
complement mediated lysis of RBC and PNH DAF deficiency
help prevent complement activation on self cells DAF and C1 esterase
produce a ribonuclease that inhibits viral protein synthesis by degrading viral mRNA interferons
cross link the beta region of the T cell receptor to the MHC class II on APCs Superantigens
causes uncoordinated release of IFNgamme from Th1 cells and then the release of IL-1, 6 and TNF alpha from macrophages superantiges
Endotoxin/LPS from G-s mechanism directly stimulate macrophages by binding to endotoxin receptor CD14
Passive immunity (preformed abs) needed Tetanus, Botulinum, HBV, Rabies
neutrophil chemotaxis IL8, C5a, LTB4
Free antigen cross links IgE on presensitized mast cells/basophiles triggering the relase of histamine Type I hypersensitivity
Scratch test and RISA Type I hypersensitivity
IgM, IgG bind to fixed antigen on "enemy" cell leading to lysis or phagocytosis Type 2 hypersensitivity
Antibody and complement lead to MAC attack Type 2 hypersensitivity
Direct and Indirect cooombs test Type 2 hypersensitivity
Antigen Antibody complexes activate complement which attracts NPs which release lysosomal enzymes Type 3 hypersensitivity
fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure serum sickness: Type 3 HS
Edema, necrosis, and activation of complemnet Arthus rxn: Type 3 HS
sensitized T lymphocyes encounter antigen and then release lymphokines (causing macrophage activation Type 4 hypersensitivity
Immunofluorescent staining Type 3 HS
Patch test (PPD) Type 4 HS
T lymphocytes, Transplant rejection ,TB skin tests, touching(contact dermatitis) Type 4 HS
antibody mediated due to preformed antidonor abs hyperacute rejection
ischemia and necrosis occluding graft vessels hyperacute rejection
cell mediated due to Tc reacting against foreign MHC; REVERSIBLE acute rejection
vasculitis of graft vessels with dense interstitial lymphocytic infiltrate acute rejection
T cell and ab mediated vascular damage: IRREVERSIBLE chronic rejction
fibrosis of graft tissue and blood vessels chronic rejection
maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea GVHD
for Hep B/C, Kaposi sarcoma, leukemias, malignant melanoma IFN alpha
for MS IFN beta
for CGD IFN gamma
Aldesleukin (IL-2) for RCC, metastaic melanoma
Filgrastim G-CSF for bone marrow recovery
Sargramostim GM-CSF for bone marrow recovery
Created by: kayjames