What are the similarities and divergences between Immunoglobulin and T-Cell Receptor (TCR) rearrangement? What are the genes and key enzymes involved in this process?
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What are the similarities and divergences between Immunoglobulin and T-Cell Receptor (TCR) rearrangement? What are the genes and key enzymes involved in this process?
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- Secondary lymphoid organs (SLOs) are important sites for the initiation of T cell responses via immune priming. Once an antigen-presenting cell (APC) presenting peptide-MHC arrives at a secondary lymphoid organ, it must find a relatively rare T cell clone with a TCR that recognizes its presented peptide-MHC complex. Which of the following features of SLOs increases the likelihood of this APC finding its cognate T cell? Activated APCs are captured by SLO-resident macrophages once they enter via afferent lymphatics, allowing them to be interrogated by T cells Concentrate high densities of T cells within specific zones to enable efficient APC browsing Drain pathogens from infected tissues through the lymphatics, bringing them to secondary lymphoid organs where they can be killed by B cells Contain specialized nutrients that are required for productive TCR signaling following interactions with a cognate APC1:Describe the various stages of T cells and the events that occur during each of these stages during T cell development. What stages of T cell development would be affected in mice with the following genetic mutations? Justify your answer. a) Mice that do not express MHC Class I molecule. b) Mice that do not express Rag1 c) Mice that do not express the pre-T-alpha chain 2:Transgenic mice that have constitutive expression of Rag1/2 are being used in an experiment to study pre-BCR signaling. Based on your knowledge of early B cell development, speculate on what might be the fate of BCR rearrangement and how will this affect further development of B cells in the bone marrow? please answer in full detail I want long well explained answers.In a set of experiments, T cells from wild-type (WT) or bm12 mice were mixed in vitro with antigen-presenting cells (APCs), in the presence or absence of the superantigen staphylococcal enterotoxin B (SEB), and T cell proliferation was measured. The data from these experiments are shown in the figure below. What is the explanation for the results in Rows 1–4 of the table?. Why does the T cell response to SEB (Rows 5–8) show a different pattern than the response to bovine insulin? Note: Epitope mapping studies identified amino acid residues 1–14 of the bovine insulin A chain as the peptide recognized by CD4 T cells from wild-type mice.
- Influenza virus causes serious disease and death, and is responsible for one of the largest pandemics in recorded history. However, the process by which antigens are made and processed are not unique to that virus. Answer the following questions to trace how infected cells will become recognizable by the TCR of a compatible T-cell. A) Where are the viral proteins made? B) Describe the process by which viral proteins are broken down into peptides. Be sure to discuss any unique molecules or organelles that participate in the process. C) Which MHC molecule presents these peptides? D) Now that you have made peptides from the viral antigen, how do they get to and bind to the MHC molecule? Describe the process. What unique molecules are involved in this process? E) What is the final destination for these molecules/epitopes, and how do they reach that destination?There are two classes of MHC molecules with distinct subunit compositions but similar three-dimensional structures. Both MHC class I and MHC class II molecules are highly polymorphic genes in the human population, with tens to hundreds of different alleles co-existing in the population. This means that a comparison of the MHC protein sequences between two individuals would reveal amino acid differences between one individual and the next. However, these amino acid differences are not randomly distributed along the entire protein, but are clustered in certain locations. In the figure below, the diagram that most correctly indicates the regions of greatest variability between different MHC proteins (shown by the red highlights) is: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…
- T cells and B cells have many similarities in how they produce their highly diverse repertoire of antigen receptors, but one important difference between them is that B cell receptors can undergo somatic hypermutation to alter their affinity for antigen. This is known as ‘affinity maturation’, and the result is that the pool of B cells specific for a particular microbe will increase their binding affinity. T cells do not engage in either somatic hypermutation or affinity maturation. What potential harm could come from allowing T cells to alter the affinity of their TCRs after they have already left the thymus and have become activated in a lymph node or spleen?For immunoglobulin heavy and light chain genes, and for T-cell receptor b chain genes, there are a large number of V gene segments, and relatively few J and/or D segments that rearrange to form the final coding sequence for each gene. The TCR a locus is different in this regard, and this difference is thought to reflect the fact that nearly all a:b T-cell receptors recognize a peptide bound to an MHC molecule. This unique feature of the T-cell receptor a locus is: The presence of only five different Va gene segments The presence of two different Ca coding sequences The presence of over sixty different Ja gene segments The absence of D gene segments The large sequence distance separating the Va gene segments from the Ja gene segmentsSurprisingly, humans as well as mice deficient in the complement protein, C3, have greatly reduced antibody responses to T cell-dependent antigens, and are impaired in their ability to control HSV infections. When C3-deficient mice are infected with HSV, once at day 0 and then a second time 4 weeks later, their antibody response is altered compared to wild-type mice, as shown in the figure #3 below. a) What is a likely explanation for the altered antibody response in the absence of complement C3? For fugure #4: For this experiment, mice are infected with varying doses of the HSV-rd virus, and peak IgG responses to the viral surface glycoproteins are measured. The results are shown in the fugure #4. b) What is the most likely explanation for these data? Do these results impact your answer to the part above (a)? Explain your reasoning.
- To avoid the potential for activating self-reactive T cells that might cause autoimmunity, naive T cell activation has stringent requirements for co-stimulatory signals in addition to the engagement of T-cell receptors with peptide: MHC complexes. Yet this requirement is abandoned once T cells have differentiated into effector cells. Name two effector T cell functions that would fail if effector T cells also required T-cell receptor signals plus co-stimulatory signals through CD28 to elicit their effector responses.Three major cell types, dendritic cells, macrophages, and B cells, present peptides bound to MHC class II molecules for recognition by CD4 T cells. In general, these peptides are derived from proteins or pathogens taken up by the cell by endocytosis, phagocytosis, or macropinocytosis. Based on these pathways of antigen uptake, some of the enzymes that degrade proteins to generate peptides for MHC class II presentation are: Ubiquitin ligases that tag proteins for degradation by the proteasome ATP transporter proteins that deliver endocytic proteins into the cytosol for degradation Cysteine proteases like cathepsins that function at acidic pH The lysosomal thiol reductase found in the endosomes The lysosome-associated membrane trafficking protein, LAMP-2How does a single MHC protein present many differentpeptides to T cells?