Anti-Mouse TIM3 Functional Grade Purified

Description: The 8B.2C12 monoclonal antibody reacts with mouse Tim-3, a Th1-specific cell surface protein. Tim-3, a type I transmembrane protein, contains an immunoglobulin and a mucin-like domain in its extracellular portion and a tyrosine phosphorylation motif in its cytoplasmic portion. Tim-3 is expressed selectively by differentiated CD4⁺Th1 and CD8⁺Tc1 cells, but is absent on CD4⁺Th2 and CD8⁺Tc2 cells. Other hematopoietic cell types, including naïve T cells, B cells, macrophages and dendritic cells, do not express Tim-3, at least at the protein level. Tim-3 expression is upregulated at a late stage of T cell differentiation on Th1 cells after 3 rounds of in vitro polarization suggesting a role for this molecule in the transport or effector function of Th1 cells rather than a contribution to T cell differentiation. In an experimental autoimmune encephalomyelitis (EAE) model, Tim-3 was shown to be expressed on most CD4⁺ and CD8⁺ T cells in the central nervous system at the onset of clinical signs of disease, while less than 2% of CD4⁺ cells in the periphery expressed Tim-3 after immunization. In this model, in vivo administration of 8B.2C12 resulted in a hyperacute and atypical disease phenotype. It is postulated that the engagement of Tim-3 during T cell activation results in the expansion and activation of macrophages and increased severity of an autoimmune disease. The Tim gene family may have an important role in the regulation of autoimmunity and allergies.

The 8B.2C12 antibody binds to the Tim-3 BALB/c allele. Reactivity to the C57/Bl6 is significantly weaker than BALB/c.

References: Monney, L., C.A. Sabatos, et al. 2002. Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease. Nature 415(6871): 536-41.

McIntire J.J., S.E. Umetsu, et al. 2001. Identification of Tapr (an airway hyperreactivity regulatory locus) and the linked Tim gene family. Nat Immunol. 2(12):1109-16.

Beauregard C, Stevens C, Mayhew E, Niederkorn JY. Cutting edge: atopy promotes Th2 responses to alloantigens and increases the incidence and tempo of corneal allograft rejection. J Immunol. 2005 Jun 1;174(11):6577-81. (IHC, PubMed)

Frisancho-Kiss S, Nyland JF, Davis SE, Barrett MA, Gatewood SJ, Njoku DB, Cihakova D, Silbergeld EK, Rose NR, Fairweather D.Cutting Edge: T Cell Ig Mucin-3 Reduces Inflammatory Heart Disease by Increasing CTLA-4 during Innate Immunity. J Immunol. 2006 Jun 1;176(11):6411-6415. (FA, PubMed)