Understanding the many biological extraskeletal actions of vitamin D has increased in the past decades. Indeed, vitamin D andanalogue molecules, besides the classical actions on bone metabolism, exert several beneficial effects on metabolic homeostasis,heart-cardiovascular, brain, and muscle physiological functions, throughout the interaction with the specific vitamin D receptor(VDR). In particular, VDR agonists powerfully control innate and adaptive immune systemwith favorable effects on human health.VDR ligands act as immunomodulators that are potent enough to retain anti-inflammatory effects, even though the mechanismunderlying those effects is not yet fully elucidated.VDR agonists exert a significant suppression of inflammatory processes switchingthe immune response from T helper 1 (Th1) to T helper 2 (Th2) dominance and counteracting the self-enhancing inflammatoryloop between immune and resident cells, especially by cytokine release impairment. Those molecules are able, indeed, to reduce therelease of the interferon (IFN)𝛾-induced 10 kDa protein IP-10/CXCL10, a powerful chemokine driving Th1-mediated inflammation.Based on their features, VDR ligands show the potentiality to be included in immunosuppressive regimens, aimed to control autoandalloimmuneTh1-driven overreactivity, occurring, for example, in autoimmune disease or graft rejection.
Vitamin D receptor agonists target CXCL10: New therapeutic tools for resolution of inflammation
Di Luigi L;Crescioli C
2013-01-01
Abstract
Understanding the many biological extraskeletal actions of vitamin D has increased in the past decades. Indeed, vitamin D andanalogue molecules, besides the classical actions on bone metabolism, exert several beneficial effects on metabolic homeostasis,heart-cardiovascular, brain, and muscle physiological functions, throughout the interaction with the specific vitamin D receptor(VDR). In particular, VDR agonists powerfully control innate and adaptive immune systemwith favorable effects on human health.VDR ligands act as immunomodulators that are potent enough to retain anti-inflammatory effects, even though the mechanismunderlying those effects is not yet fully elucidated.VDR agonists exert a significant suppression of inflammatory processes switchingthe immune response from T helper 1 (Th1) to T helper 2 (Th2) dominance and counteracting the self-enhancing inflammatoryloop between immune and resident cells, especially by cytokine release impairment. Those molecules are able, indeed, to reduce therelease of the interferon (IFN)𝛾-induced 10 kDa protein IP-10/CXCL10, a powerful chemokine driving Th1-mediated inflammation.Based on their features, VDR ligands show the potentiality to be included in immunosuppressive regimens, aimed to control autoandalloimmuneTh1-driven overreactivity, occurring, for example, in autoimmune disease or graft rejection.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
