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Havcr2  -  hepatitis A virus cellular receptor 2

Mus musculus

Synonyms: HAVcr-2, Hepatitis A virus cellular receptor 2 homolog, T-cell immunoglobulin and mucin domain-containing protein 3, T-cell immunoglobulin mucin receptor 3, T-cell membrane protein 3, ...
 
 
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Disease relevance of Havcr2

 

High impact information on Havcr2

  • Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease [1].
  • In vivo administration of antibody to Tim-3 enhances the clinical and pathological severity of experimental autoimmune encephalomyelitis (EAE), a Th1-dependent autoimmune disease, and increases the number and activation level of macrophages [1].
  • Genomic association of the TIM family and polymorphisms in both Tim-1 and Tim-3 in different immune-mediated diseases suggest that the family may have an important role in regulating immunity, both in terms of normal immune responses and in diseases like autoimmunity and asthma [7].
  • Fusion proteins (Tim-3-Ig) of both Tim-3 isoforms specifically bound CD4(+) T cells, indicating that a Tim-3 ligand is expressed on CD4(+) T cells [8].
  • These results indicate that regulation of inflammation in the heart begins during innate immunity and that Tim-3 signaling on cells of the innate immune system critically influences regulation of the adaptive immune response [5].
 

Biological context of Havcr2

  • T helper type 1 (T(H)1) immune responses are central in cell-mediated immunity, and a T(H)1-specific cell surface molecule called Tim-3 (T cell immunoglobulin domain, mucin domain) has been identified [8].
  • Our results suggest that Tim-3 may play a crucial role in the regulation of CD8(+) T cells responsible for the maintenance of hepatic homeostasis and tolerance [4].
  • The chromosome 11 QTL co-localizes with eae6b, and with Il12b and heptatitis A virus cellular receptor 2 (Havcr2, formerly known as Timd3), both of which are candidate genes for this QTL [9].
  • In this study, a cellular surface membrane protein of immunoglobulin (Ig) superfamily (IgSF) was identified from a human dendritic cell (DC) cDNA library by large-scale random sequencing, which is identical to previously reported Tim-3 (T-cell Ig- and mucin-domain-containing molecule 3) [10].
  • CONCLUSIONS: A transient upregulation of Tim-3 expression was observed in the early stage of ACAID, suggesting its possible involvement in the development of ACAID [11].
 

Anatomical context of Havcr2

  • We report here that the T(H) type 1 (T(H)1)-specific Tim-3 (T cell immunoglobulin domain, mucin domain) protein functions to inhibit aggressive T(H)1-mediated auto- and alloimmune responses [12].
  • Tim-3 ligand expression was also up-regulated in splenic T cells, DCs, and macrophages, but not in the hepatic lymphocytes [4].
  • T Cell Ig- and mucin-domain-containing molecule-3 (TIM-3) and TIM-1 molecules are differentially expressed on human Th1 and Th2 cells and in cerebrospinal fluid-derived mononuclear cells in multiple sclerosis [3].
  • PURPOSE: To assess the expression of T-cell immunoglobulin- and mucin-domain-containing molecule 3 (Tim-3) in the spleens of BALB/c mice undergoing anterior chamber-associated immune deviation (ACAID) [11].
  • Whereas lesional macrophage content, aortic CD4, and Th1-related Tim3 expression were reduced, smooth muscle cell (SMC) content and expression of interleukin-10 in plaques, lesional SMCs, and splenocytes were elevated [13].
 

Other interactions of Havcr2

  • Using real-time (TaqMan) RT-PCR, we show that human Th1 lines expressed higher TIM-3 mRNA levels, while Th2 lines demonstrated a higher expression of TIM-1 [3].
 

Analytical, diagnostic and therapeutic context of Havcr2

References

  1. Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease. Monney, L., Sabatos, C.A., Gaglia, J.L., Ryu, A., Waldner, H., Chernova, T., Manning, S., Greenfield, E.A., Coyle, A.J., Sobel, R.A., Freeman, G.J., Kuchroo, V.K. Nature (2002) [Pubmed]
  2. Dysregulated T cell expression of TIM3 in multiple sclerosis. Koguchi, K., Anderson, D.E., Yang, L., O'Connor, K.C., Kuchroo, V.K., Hafler, D.A. J. Exp. Med. (2006) [Pubmed]
  3. T Cell Ig- and mucin-domain-containing molecule-3 (TIM-3) and TIM-1 molecules are differentially expressed on human Th1 and Th2 cells and in cerebrospinal fluid-derived mononuclear cells in multiple sclerosis. Khademi, M., Illés, Z., Gielen, A.W., Marta, M., Takazawa, N., Baecher-Allan, C., Brundin, L., Hannerz, J., Martin, C., Harris, R.A., Hafler, D.A., Kuchroo, V.K., Olsson, T., Piehl, F., Wallström, E. J. Immunol. (2004) [Pubmed]
  4. Preferential Involvement of Tim-3 in the Regulation of Hepatic CD8+ T Cells in Murine Acute Graft-versus-Host Disease. Oikawa, T., Kamimura, Y., Akiba, H., Yagita, H., Okumura, K., Takahashi, H., Zeniya, M., Tajiri, H., Azuma, M. J. Immunol. (2006) [Pubmed]
  5. Cutting edge: T cell Ig mucin-3 reduces inflammatory heart disease by increasing CTLA-4 during innate immunity. Frisancho-Kiss, S., Nyland, J.F., Davis, S.E., Barrett, M.A., Gatewood, S.J., Njoku, D.B., Cihakova, D., Silbergeld, E.K., Rose, N.R., Fairweather, D. J. Immunol. (2006) [Pubmed]
  6. Th2-driven, allergen-induced airway inflammation is reduced after treatment with anti-Tim-3 antibody in vivo. Kearley, J., McMillan, S.J., Lloyd, C.M. J. Exp. Med. (2007) [Pubmed]
  7. TIM Family of Genes in Immunity and Tolerance. Kuchroo, V.K., Meyers, J.H., Umetsu, D.T., Dekruyff, R.H. Adv. Immunol. (2006) [Pubmed]
  8. Interaction of Tim-3 and Tim-3 ligand regulates T helper type 1 responses and induction of peripheral tolerance. Sabatos, C.A., Chakravarti, S., Cha, E., Schubart, A., Sánchez-Fueyo, A., Zheng, X.X., Coyle, A.J., Strom, T.B., Freeman, G.J., Kuchroo, V.K. Nat. Immunol. (2003) [Pubmed]
  9. Genetic analysis of the influence of neuroantigen-complete Freund's adjuvant emulsion structures on the sexual dimorphism and susceptibility to experimental allergic encephalomyelitis. Fillmore, P.D., Brace, M., Troutman, S.A., Blankenhorn, E.P., Diehl, S., Rincon, M., Teuscher, C. Am. J. Pathol. (2003) [Pubmed]
  10. Human membrane protein Tim-3 facilitates hepatitis A virus entry into target cells. Sui, L., Zhang, W., Chen, Y., Zheng, Y., Wan, T., Zhang, W., Yang, Y., Fang, G., Mao, J., Cao, X. Int. J. Mol. Med. (2006) [Pubmed]
  11. Expression of Tim-3 is transiently increased before development of anterior chamber-associated immune deviation. Wang, Y., Yang, P., Li, B., Zhou, H., Huang, X., Wang, Y., Chi, W., Zhu, X., Zhu, L., Kijlstra, A. Ocul. Immunol. Inflamm. (2006) [Pubmed]
  12. Tim-3 inhibits T helper type 1-mediated auto- and alloimmune responses and promotes immunological tolerance. Sánchez-Fueyo, A., Tian, J., Picarella, D., Domenig, C., Zheng, X.X., Sabatos, C.A., Manlongat, N., Bender, O., Kamradt, T., Kuchroo, V.K., Gutiérrez-Ramos, J.C., Coyle, A.J., Strom, T.B. Nat. Immunol. (2003) [Pubmed]
  13. Ccr5 but not Ccr1 deficiency reduces development of diet-induced atherosclerosis in mice. Braunersreuther, V., Zernecke, A., Arnaud, C., Liehn, E.A., Steffens, S., Shagdarsuren, E., Bidzhekov, K., Burger, F., Pelli, G., Luckow, B., Mach, F., Weber, C. Arterioscler. Thromb. Vasc. Biol. (2007) [Pubmed]
 
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