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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Antigens, CD, Antigens, Differentiation, T-Lymphocyte, Antineoplastic Agents, Benzoates, Cell Differentiation, Chromans, Cytokines, Dermatologic Agents, Fenretinide, Gene Expression Regulation, Humans, Lectins, C-Type, Lymphocyte Activation, Receptors, Retinoic Acid, Retinoic Acid Receptor alpha, Tetrahydronaphthalenes, Th2 Cells, Tretinoin, Tumor Cells, Cultured.
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Does the Retinoic Acid Receptor-alpha mediate human T-cell activation and Th2 cytokine and chemokine production? Context: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Here, we have demonstrated that the observed effects using ATRA and 9-cis RA are shared with the clinically useful RAR ligand, 13-cis retinoic acid (13-cis RA), and the retinoic acid receptor-alpha (RAR-alpha)-selective agonist, AM580 but not with the RAR-beta/gamma ligand, 4-hydroxyphenylretinamide (4-HPR). The increase in type 2 cytokine production by these retinoids correlated with the expression of the T cell activation markers, CD69 and CD38. The RAR-alpha-selective agonist, AM580 recapitulated all of the T cell activation and type 2 cytokine-inducing effects of ATRA and 9-cis-RA, while the RAR-alpha-selective antagonist, RO 41-5253, inhibited these effects.
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These results strongly support a role for RAR-alpha engagement in the regulation of genes and proteins involved with human T cell activation and type 2 cytokine production. Final Decision: yes