Sympathetic neurotransmitters such as norepinephrine predominantly bind beta2- adrenergic receptors on lymphocytes ,of adaptive immunity. These receptors are highly expressed on: OB ells CD4+ T cells
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- When a helper T cell releases interleukin-1 to stimulate surrounding leukocytes, interleukin-1 is acting as: A. paracrine B. neurotransmitter C. autocrinePentadecacatechol, a poison ivy toxin, may also activate cytotoxic CD8 T cells. Fully describe the mechanism by which this drug activates CD8 T cells *please answer the question specific to contact sensitivity to poison ivyWhen 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…
- Describe mechanisms to explain why not all of the anti-thyrotropin receptor antibodies would induce receptor activation.1. https://doi.org/10.1186/s12868-022-00692-1 (link to research) a) In the effect of mitoxantrone on histopathological changes in the brain section of the results section the authors wrote “Post-administration of mitoxantrone to sedentary and exercised groups smaller patches of demyelination with microcyst formation and lymphocytic infiltrates were seen; and bare unmyelinated axons were fewer (Figs. 3D, E, I, J and 4D, E, I, J).” Based on this quote, what is mitoxantrone doing exactly/directly? b) In the histopathological study section of the materials and methods section the authors wrote “Luxol fast blue (LFB) staining was used for assessment of demyelination in the cerebellum and brain stem and scored as described previously by Zhang et al. [21] and illustrated in Table 2.” Why was demyelination assessed in this study?Explain why each choice (a-d) is correct or incorrect. In order for an antigen to activate or sensitize a T helper cell, the antigen must be a. coated with antibodies b. displayed on the surface of an APC along with MHC antigens c. displayed on the surface of another T cell with IgD antibodies d. partly digested by a natural killer cell
- Figure shows a series of events for the response in innate immune defense. a)State ONE main event happening in J in fighting pathogens. b)Natural killer cell has the ability to kill virus-infected cells and tumour cells rapidly. How do natural killer cells in event K recognise and kill these cells?During the chemotaxis phase of the inflammatory response,a. C-reactive protein is secreted by damaged parenchymal cells in the tissue, which attracts neutrophils, which secrete leukotrienes and prostaglandins to attract macrophages; a purulent exudate is formed.b. Band cells respond to hyperthermia by producing TNF-α and interleukins, which then cause a left shift that results in the accumulation of neutrophils within the tissue.c. Damaged parenchymal cells release prostaglandins and leukotrienes to attract macrophages, causing a left shift and the formation of a purulent exudate.d. Cytokines, such as TNF-α, are released by damaged parenchymal cells, while leukotrienes and prostaglandins produced by neutrophils cause smooth muscle constriction and the further accumulation of leukocytes.The Gram-negative bacterium Yersinia pestis, thecausative agent of the plague, is extremely virulent. Uponinfection, Y. pestis injects a set of effector proteins intomacrophages that suppresses their phagocytic behaviorand also interferes with their innate immune responses.One of the effector proteins, YopJ, acetylates serines andthreonines on various MAP kinases, including the MAPkinase kinase kinase TAK1, which controls a key signalingstep in the innate immune response pathway. To deter-mine how YopJ interferes with TAK1, you transfect humancells with active YopJ (YopJWT) or inactive YopJ (YopJCA)and with FLAG-tagged active TAK1 (TAK1WT) or inactiveTAK1 (TAK1K63W), and assay for total TAK1 and for phos-phorylated TAK1, using antibodies against the FLAG tag oragainst phosphorylated TAK1 (Figure Q23–1). How doesYopJ block the TAK1 signaling pathway? How do you sup-pose the serine/threonine acetylase activity of YopJ mightinterfere with TAK1 activation?
- In a patient with Essential thrombocytemia, a mutation in JAK2 - a downstream effector of cytokine receptor, results in a constitutive activation of the pseudokinase domain of the receptor and an inhibition of signaling via this pathway. Group of answer choices True FalseThe 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!Denervation supersensitivityof the muscle in LMN lesions is due to : -a- increased release of neurotransmitter from the degenerating nerve terminalsb- decreased release of neurotransmitter from the degenerating nerve terminalsc- increased number of transmitter receptors in fibers of the denervated muscled- decreased number of transmitter receptors in fibers of the denervated muscle