3 Infliximab is a chimeric mouse-human monoclonal antibody generated against the inflammatory cytokine TNF-a. Adalimumab is a fully humanized anti-TNF-a antibody. How might some patients become resistant to infliximab therapy and yet still respond to adalimumab?
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- "Gamma-delta' T cells differ from 'alpha-beta' T cells by all of the following except O alpha-beta cells are more commonly found in skin and other tissues, while gamma-delta cells are primarily in lymph nodes. gamma-delta cells undergo more hypermutation for their receptor genes. gamma-delta cells respond more with non-peptide antigens, especially phospholipids. O production of an effector response occurs more rapidly in alpha-beta T cells.4 Natalizumab is a therapeutic monoclonal antibody that targets the cell- adhesion molecule a4-integrin and is used as a second-line therapy for severe Crohn's disease. What might be its mechanism of action?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…
- Which of the following pairs is mismatched? a. effector memory γ:δ T cells; CD45RA b. splenic γ:δ T cells; Vδ1 c. naive γ:δ T cells; CD27 d. isopentyl pyrophosphate; self phosphoantigen e. hydroxyl-methyl-but-2-enyl-pyrophosphate; BTN3A1 f. glucose monomycolate; Mycobacterium phlei.How does the design of CAR T-cell therapies address the limitation of requiring 2 signals for full T cell activation?2. Polyclonal activation of T₁ cell populations Cause: Superantigen Definition Mechanisms Consequences
- Based on the data shown in chart, titled IL-2 Response by Macrophages that express TLR-XX would you predict that cytochalasin B treatment would inhibit TLR-XX dependent anti-viral immune responses to live RNA virus, Yes or No? Why? please be as concise as possible but clear in your response.The autoimmune attack on nAChR leads to a decrease in the number of available receptors due to antibodies binding to the receptors. 2. Where could you find these antibodies binding? Choose ALL that apply. a. effectors of the parasympathetic nervous system b. effectors of the somatic nervous system c. effectors of the sympathetic nervous system d. pre-ganglionic neurons of the parasympathetic nervous system e. pre-ganglionic neurons of the sympathetic nervous system f. post-ganglionic neurons of the parasympathetic nervous system g. post-ganglionic neurons of the sympathetic nervous system PLEASE EXPLAIN YOUR REASONING!Helper T cells can be activated by macrophages(which engulf everything indiscriminately) or by B cells (which only engulf antigens that stick to their receptors). A. What properties so macrophages and B cells have ibn common that allows them both to activate T cells? B. It has been suggested that macrophages probably do most to fhte T cell activating in the primary response but B cells do most of it in the secondary response. Why does this make sense?
- 1. Basic of signal tranduction pathway in cancer disease 2. Specific of cellular response and organismal response in cancer disease.Tumor necrosis factor alpha (TNF-α) is an important cytokine used by immune cells to initiate and coordinate inflammatory responses. Inflammation is a key response to cell damage or infection, but can, in some diseases, spiral out of control and become more of a problem than the original cause (COVID-19 lung damage is a relevant example...). TNF-α receptors exist on many cell types. Let’s study the interaction between TNF-α (T) and its receptor (R), to form an activated complex C: T + R ↔ C A macrophage is measured to have ~105 TNF-α receptors on its surface. If the macrophage is immersed in a high concentration of TNF-α molecules (i.e. L0 ≅ L), how will the number of activated receptors change over time? Plot this trend for the case L0 =10 nM, kf=106 M-1 min-1, kr=0.1 min-1. There is constant ligand concentration and an initial condition of C0 = 0. We are given the constants needed to model the number of activated receptors over time and can use the following equation: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.