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Immuno Lec 3
| Question | Answer |
|---|---|
| Cytokines | T cell mediated immunity Inflammation small amounts short range action, systemic effects Pleotropic Redundancy |
| Pleotropic | Different effects on different cells |
| Redundancy | Many cytokines have overlapping functions |
| Il-1 | secreted by Monocytes/Macrophages autocrine Pyrogen B cell proliferation |
| Il-2 | Secreted by CD4+ T Cells Autocrine Proliferation and Differentation of T, B, and NK cells |
| IL-4 | Secreted by CD4+ T Cells B cell proliferation, 2nd signal. Class Switching |
| IL-7 | Secreted by Thymic Cortical Epithelial Cells Bone Marrow Stromal Cells T/B Cell proliferation during development |
| Interferon alpha and beta | Secreted by all Cells (Monos, fibroblasts) Induces antiviral state Activates NK cells |
| Interferon Gamma | Secreted by T Cells, NK cells class switching, Ig2, 3, Mac |
| Chemokines | secreted by many cell types cc -attracts monos and T cells cxc - attracts neutrophils (Il-8) |
| TNFa | Secreted by many cell types Directly kill tumor cells activates monocytes/macs expression of Adhesion molecules |
| TNFb | Secreted by T and B cells directly kill tumor cells activate monocytes/macs Expression of adhesion molecules |
| Emigration/Extravasion of Naive T cells into 2* Lymphoid Tissue | Mediated by adhesion molecules. Four step process, endothelial cells express P-selectin and E-selectin |
| 4 steps of emigration of naive T cells into 2* lymphoid tissue | Rolling adhesion - P/E selectins bind to L selectin found on circulating leukocytes Tight binding - further interaction between integrins (LFA-1 and ICAM1) causes it to stop. Diapedesis Migration |
| Diapedesis | Travel across membrane |
| Migration | Travels to site |
| Antigen Presenting Cells | Occurs during migration to T cell areas. Macrophages, B cells, Dendritic Cells |
| What activates Macrophages on the way to T cell areas | Bacterial/Viral cell wall components |
| CD4+ Cell Activation | Two Steps. 1)Ag/MHCII. In 2* lymphoid tissue, macrophage has engulfed extracellular pathogen, TCR reacts with it. 2) Mac comes into contact with Toll Length Receptor on pathogen, then expresses IL-1 and B-7. B-7 engages with CD28 and IL-1 is secreted. |
| What does the 2 signal requirement for T cell activation ensure | peripheral tolerance |
| What if the T cell only gets signal 1? | The T cell becomes anergic. It is not responsive to antigen. It may die. If it contacts self antigen(signal 1), but no infection, signal 2 (B7 and IL1 wont be there). |
| Superantigen | Non-antigen specific stimulation of T cells. not processed Bind MHCII, Vb domain of TCR. Exception to rules. binds externally, it is outside, specificity requirement eliminated. Activates ALOT of T-Cells, massive cytokine release. fever,death,etc. |
| Naive CD4+ Cell can become what | ARMED EFFECTOR CELLS : TH1 and TH2, needs Both Signals Still. |
| TH1 | In Presence of IL-12, IFNy, TGFb. Secretes IL2, IFNy, TNFb. Inflammatory cells, activate CD8, Macro, NK cells. Cell Mediated Immunity. recruit neutrophils. Mediate Delayed Type Hypersensitivity. |
| TH2 | In presence of IL-4 and IL-10. Helper Cells. Humoral immunity(Abs produced). Secrete IL4,5,6,13. Important for activation, differentiation, proliferation of B cells into plasma cells. Provide Signal for Class Switching. Mast/Eos Activation. |
| Difference between Armed Effector Cells and Naive T Cell | Armed effector cells no longer need both signals. They only need the TCR to engage p/MHCII. this reactivates it. |
| Specific delayed type hypersensitivity | specific CD4+ T cells encounter microbes. Requires proper antigen. |
| Non-specific delayed type hypersensitivity | If you have mixed infection, activated macrophages that not specific. will engulf any bystander. produce free radicals and NO, potent Antibacterial activity, damaging to host. |
| Il-5 | Activates eosinophils |
| CD8+ Activation | 2 Signals. Antigen/MHCI B7/IL-1 OR IL-2 activated by langerhan cells. Cd-28 T cell marker. |
| Langerhan Cells | Located below epithelial surface. takes microbes to 2* lymphoid organs. Once effector cells are activated, they go back to site. |
| CTL Mechanism | cytoskeletal reorganization causes granules to concentrate near target cell, exocytosis of granules containing perforin, death by osmotic lysis/apoptosis. |
| DiGeorge Syndrome | Thymic aplasia. no functional thymus. absence of parathyroid gland. no T cell mediated immunity Greatly reduced serum Ig Since you require TH2 to activate B cells, lose those too. |
| Severe Combined Immunodeficiency | SCID. lack of cell mediated and humoral immunity. mutation in gamma chain of IL-2. |
| Wiscott Aldrich Syndrome | Loss of CD43. WASP protein. do not divide properly. do not mature properly. severely impaired cell mediated and humoral immunity. |
| Mucocutanous Candidiasis | defect in T cell immunity infections of skin, nails, mucous membranes. |
| Human Immunodeficiency Virus Infection | AIDS. retrovirus. infects CD4+ cells. gradual decrease in CD4+ cells, breakdown of immune response. Infection with opportunistic organisms. |
| HIV typical cousse. | Three stages. 1*, Latency, AIds. Cd4+ cells drop continuously. anti-Hiv antibody peaks during latency. Virus in blood Peaks in 1*, settles down, then increases during Aids. |