Describe in detail the effect of loss or mutation of LAT & Blk of the following molecules/proteins/genes/domains in immune signaling. Be sure to include the normal function and the function effected by the mutation. Include all relevant players and their roles. You may use diagrams if needed.
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Describe in detail the effect of loss or mutation of LAT & Blk of the following molecules/proteins/genes/domains in immune signaling. Be sure to include the normal function and the function effected by the mutation. Include all relevant players and their roles. You may use diagrams if needed.
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- When T cells are activated by recognizing peptide:MHC complexes on dendritic cells in the lymph node, they up-regulate the receptor CD69. For T cells expressing a given T-cell receptor, the initial strength of the T-cell receptor signal can be modulated by varying the number of peptide:MHC complexes on the dendritic cells, or by varying the affinity with which the T cell-receptor binds to the peptide:MHC complexes. As a result, T cells stimulated with stronger T-cell receptor signals will maintain high expression of CD69 for one or two days longer that if those same T cells were stimulated with weaker T-cell receptor signals. Therefore, T cells stimulated with weaker T-cell receptor signals are likely to: Die by apoptosis Undergo more rounds of proliferation that T cells stimulated with stronger T-cell receptor signals Migrate to the B-cell zones of the lymph node Have reduced effector functions, such as cytokine production Egress from the lymph node 1–2 days earlier than T cells…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.TLRs activate NFkB, AP-1, and IRF transcription factors to induce the expression of inflammatory cytokines and type I interferons. A key feature of TLR signaling is the ability to induce inflammatory cytokine gene expression extremely rapidly following TLR stimulation. This is accomplished by signaling pathways using several mechanisms to activate transcription factors that are already present in the cell prior to TLR stimulation, but are kept in an inactive state. These signaling pathways use all of the following mechanisms EXCEPT: Induced ubiquitination leading to protein degradation Induced ubiquitination inducing protein–protein interactions Induced phosphorylation leading to nuclear translocation Induced phosphorylation leading to kinase activation Induced phosphorylation preventing protein degradation
- A mutant B cell line is examined by confocal microscopy after incubation with a microbial pathogen recognized by the BCR on these B cells. The B cells have been stained with antibodies to visualize the localization of polymerized actin and microtubules. As a control, wild-type B cells are examined. The results are shown in the figure below, with the numbers indicating the proportion of cells examined that show each pattern of staining. To identify the specific signaling defect in these mutant B cells, a reasonable biochemical assay would be to: Determine if BCR stimulation of mutant B cells produces enhanced binding of the B cell to the microbe Determine whether the mutant B cells have reduced levels of the enzyme Protein kinase C-q Determine whether the mutant B cells are overexpressing the enzyme Vav Determine whether BCR stimulation of mutant B cells promotes exchange of GDP for GTP on cdc42 Determine whether BCR stimulation of mutant B cells produces increased levels of DAGExplain the signaling cascade system in breast cancer by hereditary factor BRAC1, BRAC2 and hormonal factor RE, RP. Include the phases of reception, transduction, amplification and response. Also, briefly describe how the design of CAR-T killer cells can counteract cancer cells.Give an overview of the pathway and what it does, and explain the nature of the TNF ligand and the receptor for that ligand. Make sure to include an explanation of the proteolytic and phosphorylation cascades.
- Biologic agents can block cell migration to sites of inflammation and reduce immune responses. Natalizumab is a humanized monoclonal antibody directed at the a4-integrin protein, a subunit of VLA-4, the binding partner of VCAM-1 expressed on endothelium in the central nervous system, and of a4b-integrin, the binding partner of MadCAM-1 expressed on endothelium in the gut. While natalizumab has had great success in alleviating the symptoms of autoimmune diseases such as multiple sclerosis and Crohn’s disease, a small number of patients have acquired life threatening infections of the neurotrophic virus, JC. Why are patients on natalizumab particularly susceptible to a virus infection of the central nervous system?Use the SGF-signaling pathway image as a reference, to answer the following questions. Use the data provided to EXPLAIN if the cell will get to the response step or not. Keep in mind the purpose of this pathway is to cause skin cell division Growth Factor (GF-signal) Activation of GF Receptor (RTK-receptor) To cause Cell proliferation/cell division (Response) Plasma membrane Sos Grb2 (Ras GEF) (adapter) Raf МАРКK Mek МАРКK Activation of target genes that stimulate proliferation Erk МАРК You have a skin cell in a dish and have added Neural Growth Factor (NGF) to the cell media (the liquid the cell needs to live).T-cell receptors concentrate diversity in the third hypervariable region. For alpha:beta T-cell receptors, sequence diversity is heavily concentrated at the junctions formed by the rearrangement of gene segments during the generation of the expressed Va and Vb regions. The result of this organization is to position the most variable part of the T-cell receptor over a certain region of the ligand recognized by this receptor. Which region (outlined in red in figure below) indicates this part of the ligand recognized by the T-cell receptor?
- Binding of TGF-β to its receptors can elicit a variety of responses in different cell types. For example, TGF-β induces plasminogen activator inhibitor 1 in epithelial cells and specific immunoglobulins in B cells. In both cell types, Smad3 is activated. Given the conservation of the signaling pathway, what accounts for the diversity of the response to TGF-β in various cell types?It is often helpful to draw a complicated pathway in the form of a flow chart to visualize the multiple steps and the ways in which the steps are connected to each other. Draw the antibody-mediated immune response pathway that acts in response to an invading virus.Neutralizing antibodies are effective at preventing infection or toxicity mediated by pathogens or their toxic products. In fact, nearly all vaccines currently in use function by eliciting neutralizing antibodies. One example is the tetanus vaccine, in which neutralizing antibodies are generated against an inactivated form of the tetanus toxin (the tetanus toxoid). The most important feature of a neutralizing antibody is having high affinity for the antigen. being efficient at activating the complement cascade. having a high degree of multivalency, such as being a pentamer or hexamer of immunoglobulin monomers. being present at a high concentration in the circulation. 0 0 0 0