1,721,087 research outputs found
Use of kynurenine and its derivatives in the prevention and treatment of type 1 diabetes
Aryl Hydrocarbon Receptor-Dependent Pathways in Immune Regulation
The idea of a possible involvement of the Aryl hydrocarbon Receptor (AhR) in transplant tolerance can be traced back to more than thirty years ago, when Clark and coworkers found that very low doses of dioxin, the most potent AhR ligand, markedly reduced the generation of cytotoxic T lymphocytes in response to alloantigen challenge in vivo. AhR is, indeed, a ligand-activated transcription factor that is activated by dioxins and other environmental pollutants. We now know that AhR can bind a broad variety of activating ligands, disparate in nature, including endogenous molecules and those formed in the gut from food and bacterial products. Therefore, in addition to its classical role as a toxicological signal mediator, AhR is emerging as a transcription factor involved in the regulation of both innate and adaptive immune responses in various immune cell types, including lymphocytes and antigen-presenting cells. Allograft rejection is mostly a T-cell-mediated alloimmune response, initiated by the recognition of alloantigens presented by donor and recipient antigen-presenting cells to recipient CD4+ and CD8+ T cells. Based on those findings, AhR may function as a critical sensor of the outside/inside environments, leading to changes in the immune system that may have relevance in transplantation
Deciphering the lexicon between fungi and mammalian innate immunity along the kynurenine pathway
Indoleamine 2,3-dioxygenase in infection: the paradox of an evasive strategy that benefits the host.
Initially recognized in infection because of antimicrobial activity ('tryptophan starvation'), indoleamine 2,3-dioxygenase (IDO) is widely involved in host immune homeostasis and even immune evasion by microbes that establish commensalism or chronic infection. This review deals with recent findings that could gain IDO a reputation of Jack-of-all-trades in mammalian host/microbe interactions
A TLR9/TRIF PATHWAY INDUCES TOLERANCE VIA TGF-β AND TRYPTOPHAN CATABOLISM IN PLASMACYTOID DENDRITIC CELLS
IL-17 and therapeutic kynurenines in pathogenic inflammation to fungi.
Largely viewed as proinflammatory, innate responses combine with adaptive immunity to generate the most effective form of antifungal resistance, and T cells exercise feedback control over diverse effects of inflammation on infection. Some degree of inflammation is required for protection, particularly in mucosal tissues, during the transitional response occurring between the rapid innate and slower adaptive response. However, progressive inflammation worsens disease and ultimately prevents pathogen eradication. IDO, tryptophan catabolites ("kynurenines"), and regulatory T cells help to tame overzealous and exaggerated inflammatory responses. In this context, IL-23 and the Th17 pathway, which down-regulate tryptophan catabolism, may instead favor pathology and serve to accommodate the seemingly paradoxical association of chronic inflammation with fungal persistence. Recent data support a view in which IL-23/IL-17 antagonistic strategies, including the administration of synthetic kynurenines, could represent a new means of harnessing progressive or potentially harmful inflammation
Evaluation of New Extraction Procedure for Obtaining Pure Lycopene from Tomato (Lycopersicon esculentum Mill.)
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