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- The white blood cells known as T lymphocytes respond to antigens thatbind specifi cally to the T cell receptor, which consists of an antigen-binding αβ transmembrane protein as well as a set of transmembrane signaltransducing proteins known as CD3 that are targets of NRTKs. Thecytoplasmic domains of the CD3 proteins are positively charged and, in the absence of antigen, interact with the intracellular surface of the plasma membrane in such a way that buries several of their Tyr residues in the lipidbilayer. Antigen binding to the T cell receptor leads to a localized infl ux ofCa2+ ions. (a) Explain how a high concentration of Ca2+ could promote phosphorylation and activation of the CD3 proteins. (b) Would this henomenon make the T lymphocyte more or less responsive to the antigen?Innate lymphoid cells (ILCS) , implicated in tissue repair and maintenance of barrier integrity, are present in large numbers in the intestine which is also innervated by intestinal nervous system (ENS). Reccent research has shown that ILCS- express receptors for IgG express receptors for neuropeptides and neurotransmitters O function through pattern recognition receptors (PRRS) such as TLRSFor 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…
- At first glance, it would seem a dangerous strategyfor the thymus to actively promote the survival, matura-tion, and emigration of developing T cells that bind weaklyto self peptides bound to self MHC molecules. Would itnot be safer to get rid of these T cells, along with those thatbind strongly to such self-peptide–MHC complexes, as thiswould seem a more secure way to avoid autoimmune reac-tions?Chimeric mice are generated where approximately 50% of the cells in the animal are genetically MHC class I-deficient. The other 50% are deficient for the herpes virus receptor, HVEM, but do express MHC class I molecules. When these mice are infected with herpesvirus by intraperitoneal injection, a robust virus-specific CD8 T cell response is detected at day 7 post-infection in the spleens of the infected mice. Which cells are presenting herpesvirus antigens to prime the CD8 T cell response, and how did they acquire the viral antigens?Which statements are true? Explain why or why not.1 T cells whose receptors strongly bind a self-pep-tide–MHC complex are killed off in peripheral lymphoidorgans when they encounter the self peptide on an anti-gen-presenting dendritic cell. 2 To guarantee that the antigen-presenting cells inthe thymus will display a complete repertoire of self pep-tides to allow elimination of self-reactive T cells, the thy-mus recruits dendritic cells from all over the body. 3 The antibody diversity created by the combinato-rial joining of V, D, and J segments by V(D)J recombinationpales in comparison to the enormous diversity created bythe random gain and loss of nucleotides at V, D, and J join-ing sites.
- Activation of which of the following do not cause phagocytosis to occur O Pattern Recognition Receptors O Fc Receptors O B-Cell Receptor T-Cell Receptor"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.Gerintic mutuations in thhe CDda gene uften reeult ir a CD4 T.cell desciency Which of the following scenarios would be most fikely to accur in e pallent with teveral hactri Oa This patent would be less abla to produce a humotal response against various pathogenic microorganisms O b. This patient would not ba able to giroduce memory calls OE This patient would be unable to taper of the immune response folowing pathogen clearance, leading to chronic infammating Od. This piatient wauld be unable to tespond ts certain vit al invaders such as Epstein Barr Vinus QUESTION 24 The adaptive imrmine system's ability to target a particular path ogen is know as: Ca specificity O b. opsonization O. variolation d memoly QUESTION 25 Which of the following is the site on the igG foe complement bindng in the classical pathway? O a. CH2 + CH2 Oh. CH3 + CH3 OG VL- VH O d. CL + CHT
- There are several important mechanisms for generating diversity in immunoglobulin and T cell receptors. Explain the similarities and differences in mechanisms that generates diversity in these receptors.Gram negative cell walls contain lipopolysaccharide (LPS) as a unique component. All of the following apply to LPS EXCEPT O LPS is composed of mycolic acids that protect the cell from phagocytosis LPS is a PAMP that can be recognized by toll-like receptors (TLRS) as a foreign molecule fo rphagocytosis O LPS can be a target for specific IgG for ADCC-opsonization LPS can be recognized by B cells in the aosence of MHC molecules All of the answers apply, no exception O LPS is found in the outer membrane of Gram negative cellsBased 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.