Tim-3 and Tim-4 as the potential targets for antitumor therapy

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The role of TIM-containing molecules in airway disease and their potential as therapeutic targets

T cell immunoglobulin and mucin-domain (TIM)-containing molecules have emerged as promising therapeutic targets to correct abnormal immune function in several autoimmune and chronic inflammatory conditions. Despite the initial discovery linking TIM-containing molecules and the airway hyperreactivity regulatory locus in mice, there is a paucity of studies on the function of TIM-containing molecu...

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TIM-1 and TIM-3 enhancement of Th2 cytokine production by mast cells Short title: Role of TIM-1 and TIM-3 in mast cell function

Members of the T cell immunoglobulinand mucin-domain-containing molecule (TIM) family have roles in T cell-mediated immune responses. TIM-1 and TIM-2 are predominantly expressed on Th2 cells, whereas TIM-3 is preferentially expressed on Th1 and Th17 cells. We found that TIM-1 and TIM-3, but neither TIM-2 nor TIM-4, were constitutively expressed on mouse peritoneal mast cells and bone-marrow-der...

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Immune regulation by Tim-3

T-cell immunoglobulin and mucin domain 3 (Tim-3) is a transmembrane protein that in both mice and humans has been shown to possess various functions in a context-dependent manner. Thus, Tim-3 has been associated with both inhibitory and co-stimulatory function, depending in part on the specific cell type and immune response course. Though originally described on T cells, Tim-3 is now known to b...

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Mast cell activation is enhanced by Tim 1 : Tim 4 interaction but not by Tim - 1 antibodies

Polymorphisms in the T cell (or transmembrane) immunoglobulin and mucin ( ) gene, particularly in the mucin domain, have been associated domain 1 TIM-1 with atopy and allergic diseases in mice and human. Geneticand antibody-mediated studies revealed that Tim-1 functions as a positive regulator of Th2 responses, while certain antibodies to Tim-1 can exacerbate or reduce allergic lung inflammatio...

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The TIM-1:TIM-4 pathway enhances renal ischemia-reperfusion injury.

CD4+ T cells contribute to the pathogenesis of ischemia-reperfusion injury, which is the primary cause of delayed graft failure after kidney transplantation. The TIM-1:TIM-4 pathway participates in the activation/differentiation of CD4+ T cells, suggesting that it may modulate ischemia-reperfusion injury. Here, we studied the role of TIM-1 in a murine uninephrectomized renal ischemia-reperfusio...

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ژورنال

عنوان ژورنال: Human Vaccines & Immunotherapeutics

سال: 2015

ISSN: 2164-5515,2164-554X

DOI: 10.1080/21645515.2015.1056953