Mice lacking IL-15 or the IL-15Ra chain have substantially reduced numbers of type b IELS, including both a:B and y:ó T-cell receptor-positive subsets. Normal numbers of type b IELS can be restored in il15/- mice by cell-type specific expression of JL-15 in Thymic cortical epithelial cells O Thymic medullary epithelial cells O Dendritic cells O Intestinal epithelial cells

Mice lacking IL-15 or the IL-15Ra chain have substantially reduced numbers of type b IELS, including both a:B and y:ó T-cell receptor-positive subsets. Normal numbers of type b IELS can be restored in il15/- mice by cell-type specific expression of JL-15 in Thymic cortical epithelial cells O Thymic medullary epithelial cells O Dendritic cells O Intestinal epithelial cells

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 12RQ: Histamine binds to the H1 G-protein-linked receptor to initiate the itchiness and airway...

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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?
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?
T-cell receptor signaling leads to enhanced integrin-mediated cell adhesion. T-Cell Receptor stimulation was shown to affect ICAM-1 (integrin ligand) binding to LFA-1 (integrin) on T cells. To demonstrate this, varying concentrations of purified ICAM-1 were added to unstimulated or T-Cell Receptor-stimulated T cells, and the amount of ICAM-1 binding was measured. The data from such an experiment are displayed on the figure below. Please assign the red or blue lines correctly to ‘unstimulated’ or ‘T-Cell Receptor-stimulated’ T cells, and explain the reasoning for your answer.
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:
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…
Consider the following simplifieddiagram of a signal transductionpathway that regulatesprogrammed cell death inmammalian cells. Assume that thisdiagram represents the behavior ofa single cell within an organism.Key: TNF and SF are circulatingin the plasma; TNFR = TNFreceptor; SFR = SF receptor.Based on the regulatory networkdescribed above, state whethermutations that knockout each ofthe following proteins would either increase apoptosis or decrease apoptosis. TNF Bcl2 INH EFF SFR AKT TNFR SF
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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.
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The 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
Can anyone suggest a way of increasing phosphorylation of IKK alpha (Ser176/180)? Any potent phosphatase inhibitor in combination with TNF alpha?
Histamine binds to the H1 G-protein-linked receptor to initiate the itchiness and airway constriction associated with an allergic response. If a mutation in the associated G-protein’s alpha subunit prevented the hydrolysis of GTP how would the allergic response change? More severe allergic response compared to normal G-protein signaling. Less severe allergic response compared to normal G-protein signaling. No allergic response. No change compared to normal G-protein signaling.