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FA random immune
| Question | Answer |
|---|---|
| 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
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