Which of the following stages of T cell development would be affected in mice that have a genetic modification and do not express AIRE? CD4 SP and CD8 SP DN3 and DN4 DP DN1 and DN2 O O O O
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Introduction :-
T cells are a type of white blood cell that play a critical role in the immune system. They are produced in the bone marrow and mature in the thymus gland. T cells are involved in cell-mediated immunity, which is the branch of the immune system that targets infected or abnormal cells within the body.
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- Class switching is initiated by T-cell activation via CD40 ligation. You are working with a mouse model that is deficient in CD40L. What kind of phenotype would you expect to see in the mouse? a lack of memory T cells a lack of antibodies of classes other than IgM extremely high concentrations of IgE extremely low concentrations of IgDWhich of the following is MOST critical for the activation of naïve T cells during priming by DCs? Signaling through both the TCR and the co-stimulatory receptor CD28 Recognition of antigen by CD4 or CD8 molecules The presence of a chemokine gradient Production of TNFalpha by DCs as a result of their exposure to PAMPS or DAMPS Affinity maturationNaive T cells in CD69-knockout mice might: Group of answer choices Have a defect in recognizing antigen on activated dendritic cells Not be detained in the lymph node to get activated Have a defect in lymph node entry and accumulate in the blood Have a defect in responding to inflammatory cytokines in the lymph node Remain trapped in lymph nodes and fail to recirculate asap please.
- The mechanism of cross-presentation by dendritic cells is an essential pathway for generating CD8 T cell responses to some intracellular pathogens. If this pathway did not exist, we would be highly susceptible to: Intracellular pathogens that can survive inside macrophage endocytic vesicles Intracellular pathogens that are able to evade antibody responses Intracellular pathogens that do not infect and replicate in dendritic cells Intracellular pathogens that can spread from cell to cell by inducing cell fusion Intracellular pathogens that infect and replicate in red blood cellsWhich of the following is not associated with killing by a cytotoxic T cell? View Available Hint(s) for Part A granzyme CD95 perforin IL-4Which two events are required to activate a cytotoxic T cell? There is more than one answer. O Class II MHC molecules present extracellular antigen for binding on a complementary cytotoxic T cell receptor. O IL-4 is released by a TH1 cell to be bound by a cytotoxic T cell. O Class I MHC molecules presents intracellular antigen for binding on a complementary cytotoxic T cell receptor O IL-2 is released by a TH1 cell to be bound by a cytotoxic T cell.
- Describe the relationship of the following term using short terms: Negative selectionNK cellPositive selectionRegulatory T cellSphigosine-1-phosphate (S1P)Sphigosine-1-phosphate receptor (S1PR1)ThymusDuring the early developmental stages of α:β T cells in the thymus, there are two key checkpoints that must be satisfied to permit the progression of T-cell development. Explain what occurs at each checkpoint.1. Which of the following statements about CD4+ Th17 cells are true? i. Cannot form T effector memory (TEM) T cell populations ii. Require the master transcription factor RORgammaT for their development iii. Produce effector cytokines IL-17 and IL-22 which help recruit neutrophils and stimulate antimicrobial peptide production iv. Do not require the transcription factor NFAT for IL-2 production downstream of TCR activation v. Important for defense against intracellular bacterial infection only a. i and iii b. ii and v c. ii and iii d. ii, iii, iv e. i, ii, and iv
- How does the design of CAR T-cell therapies address the limitation of requiring 2 signals for full T cell activation?Cytotoxic effector T cells also produce inflammatory cytokines such as IFN-g and TNF-a when their T-cell receptor recognizes peptide:MHC on a target cell. One effect of this cytokine secretion is to enhance the ability of CD8 effector T cells to recognize and kill other infected cells in the nearby vicinity. This enhanced activity is due to: The increased production of perforin and granzymes by CD8 cells The up-regulation of MHC class I protein expression by IFN-g The ability of TNF-a to induce vascular leakage The effect of cytokines on promoting target cell apoptosis The effect of IFN-g to enhance viral replication leading to increased viral antigen presentationThe 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 mice
