599 resultados para Antígenos CD3


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Tesis (Maestría en Ciencias con Especialidad en Microbiología Médica) UANL

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Tesis (Maestría en Ciencias con Especialidad en Inmunobiología) UANL

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Tesis (Maestría en Ciencias con Especialidad en Inmunobiología) UANL

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Tesis (Maestría en Ciencias, con especialidad en Microbiología Médica) U.A.N.L.

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Tesis (Maestría en Ciencias con Orientación en Farmacia) UANL, 2012.

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Tesis ( Doctorado en Ciencias con Especialidad en Biotecnología) UANL

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Tesis ( Doctorado en Ciencias con Especialidad en Microbiología) UANL

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Tesis (Doctorado en Ciencias con Especialidad en Microbiología) UANL

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Tesis (Doctorado en Ciencias con Orientación en Inmunología) UANL, 2013.

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Absolute intensity measurements have been made on the fundamental vibrations of methyl chloride, bromide, and iodide, and their fully deuterated derivatives, by integrating the optical density over the absorption bands. The bands were fully pressure broadened by using up to 80 atmos of foreign gas. Band separations were made graphically. The results are analyzed in terms of the dipole moment derivatives with respect to symmetry coordinates in the molecule, (∂p/∂Si). The data on the different isotopic species are shown to yield consistent results, and this requirement of consistency has also been used as an aid in the analysis. In the E‐class vibrations the signs of the dipole moment derivatives have been determined unambiguously by assuming the permanent dipole to be directed CH3+☒X—.

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Antigen-presenting cells (APCs) control T-cell responses by multiple mechanisms, including the expression of co-stimulatory molecules and the production of cytokines and other mediators that control T-cell proliferation, survival and differentiation. Here, we demonstrate that soluble factor(s) produced by Toll-like receptor (TLR)-activated APCs suppress activation-induced cell death (AICD). This effect was observed in non-stimulated APCs, but it was significantly increased after lipopolysaccharide (LPS) treatment. Using different KO mice, we found that the LPS-induced protective factor is dependent on TLR4/MyD88. We identified the protective factor as prostaglandin E-2(PGE(2)) and showed that both APC-derived supernatants and PGE(2) prevented CD95L upregulation in T cells in response to TCR/CD3 stimulation, thereby avoiding both AICD and activated T cell killing of target macrophages. The PGE(2) receptors, EP2 and EP4, appear to be involved since pharmacological stimulation of these receptors mimics the protective effect on T cells and their respective antagonists interfere with the protection induced by either APCs derived or synthetic PGE(2). Finally, the engagement of EP2 and EP4 synergistically activates protein kinase A (PKA) and exchange protein directly activated by cAMP pathways to prevent AICD. Taken together, these results indicate that APCs can regulate T-cell levels of CD95L by releasing PGE2 in response to LPS through a TLR4/MyD88-dependent pathway, with consequences for both T cell and their own survival.