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- Why is this ligand for the NK-cell receptor CD94:NKG2A. considered a broad mechanism for the NK-cell detection of unhealthy cells that is relatively insensitive to MHC class I polymorphisms?What is the basic difference between the ligands recognized by CD94:NKG2A compared with inhibitory killer-cell immunoglobulin-like receptors (KIRs)?(74) A rare from of immunologic syndrome is assciated with recurrent skin lesions, eosinophilia, and increased serum concentrations of IgE. In patients with this syndrome , which of the following cytokines is most likely to be increased? (A) Interleukin-1 Beta( Il-1B) (B) Interleukin-2 ( IL-2) (C) Interleukin-4 (IL-4) (D) Interleukin-6 (IL-60 (E) Tumor Necrosis Factor alpha
- a.What would happen if IKKbeta did not phosphorylate IkappaB? b.Why is it so hard to make cytokine therapies? c.Why would you use the MyD88 independent pathway versus the MyD88 dependent pathway?Cyclosporin A and rapamycin are each used as T cell immunosuppressants. They share the property of binding to immunophilin molecules in T cells as the initial step in their mechanisms of action. However, in the case of cyclosporin A, the drug:immunophilin complex binds to and inhibits the protein phosphatase calcineurin, whereas the rapamycin:immunophilin complex binds to and inhibitors mTOR. As a consequence, Cyclosporin A, but not rapamycin, blocks cytokine production by T cells. Both cyclosporin A and rapamycin block cytokine production by T cells. Rapamycin, but not cyclosporin A, blocks T cell proliferation. Neither rapamycin nor cyclosporin A block T cell proliferation. Both cyclosporin A and rapamycin inhibit co-stimulatory signaling through CD28 on T cells.Explain the signifi cance of the observation that peptides such as fMet-Leu-Phe “activate” the phagocytotic (particle-engulfi ng) functions of mammalian leukocytes (white blood cells).
- Some viruses have mechanisms to down-regulate MHC class I protein expression on the surface of cells in which the virus is replicating. This immune evasion strategy might prevent effector CD8 cytotoxic T cells from recognizing and killing the virus-infected cells. Would this immune evasion strategy also prevent the initial activation of virus-specific CD8 T cells? Yes, because no viral peptide:MHC class I complexes would form to activate CD8 T cells. No, because dendritic cells would take up infected cells and cross-present viral peptides to activate CD8 T cells. No, because some presentation of MHC class I complexes with viral peptides would occur before the virus could down-regulate all the surface MHC class I protein. Yes, because this immune evasion strategy would also function in dendritic cells, even if the virus doesn’t replicate in dendritic cells. No, because the type I interferon response induced by the virus infection will up-regulate MHC class I expression and override the…Alefacept is a fusion protein that contains the CD2-binding domain of LFA3 fused to human IgG1, and it is used to block CD2 function on human T cells. In addition, following in vivo administration, alefacept was also shown to deplete T cells of the effector or memory subsets that express high levels of CD2. Surprisingly, clinical trials data indicated that patients on alefacept still retained responses to vaccination. For example, one set of data showed that patients on alefacept made similar responses as the control group to a vaccine designed to protect against pneumococcal disease, which is composed entirely of bacterial polysaccharide antigens (pneumococcal polysaccharide vaccine; PPV). This normal response to PPV by patients on alefacept is not surprising because: Alefacept is not very effective at blocking T cell responses. CD2 is not required for all T cell responses to vaccination. Alefacept does not deplete all effector or memory T cells, just a subset. T cells are involved…For many years it was a complete mystery howcytotoxic T cells could see a viral protein that seemed to bepresent only in the nucleus of the virus-infected cell. Theanswer was revealed in a classic paper that took advan-tage of a clone of T cells whose T cell receptor was directedagainst an antigen assoicated with the nuclear protein ofthe 1968 strain of influenza virus. The authors of the paperfound that when they incubated high concentrations ofcertain peptides derived from the viral nuclear protein, thecells became sensitive to lysis by subsequent incubationwith the cytotoxic T cells. Using various peptides from the1968 strain and the 1934 strain (with which the cytotoxic Tcells did not react), the authors defined the particular pep-tide responsible for the T cell response (Figure Q24–1).A. Which part of the viral protein gives rise to thepeptide that is recognized by the clone of cytotoxic T cells? Why do not all viral peptides sensitize the target cells forlysis by the cytotoxic T…
- An experiment is performed in a mice and studies have indicated that Batf3-/- mice lack one particular subset of conventional dendritic cells, known as CD8a+ dendritic cells (DC), but otherwise appear to have normal numbers and subsets of all other immune cell populations (e.g., T cells, B cells, macrophages, etc.). The results of this experiment are shown in the figure below. Name two possible functions of CD8a+ dendritic cells that could account for the results seen in the Batf3-/- mice immunized with WNV.The TNF family of cytokines and their receptors are critical for the development of secondary lymphoid organs, such as the lymph nodes and Peyer’s patches. As a consequence, knockout mice lacking expression of LT-b fail to develop most of these structures. Reconstitution of irradiated LT-b-deficient mice with bone marrow stem cells from wild-type mice (e.g., LT-b-sufficient) would: Restore all missing lymphoid structures in the recipient mice Restore the missing lymphoid structures but not the missing follicular dendritic cells in the recipient mice Restore the missing follicular dendritic cells but not the missing lymphoid structures in the recipient mice Have no effect on any lymphoid structures in the recipient mice Only restore the proper organization of B cell follicles in the recipient miceWhy would be the advantage of the system described for HCMV? In other words, why would decreasing NKG2D ligands and increasing HLA-E on the cell surface be advantageous over just down-regulating the expression of class I HLA?