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Gene Review

RT1-A  -  RT1-region, class I (A)

Rattus norvegicus

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Disease relevance of RT1-A

  • Several genes, including those encoding keratin K7 and the u haplotype of MHC class I RT1-A, were found to be overexpressed in neu-initiated carcinomas as well as in mammary carcinomas induced by other agents, when compared to their expression in normal mammary tissue [1].
  • In this report, we present data from two breeding studies utilizing the r8 haplotype (RT1AaBuDuEuCu) that demonstrate that (1) the RT1A locus is not involved in the disease association, (2) the MHC genes determining disease susceptibility are not unique to the BB rat, and (3) IDDM resistance genes are found outside the MHC [2].

High impact information on RT1-A

  • This antigen system is unusual in several respects: it does not involve class I RT1A gene products usually used by killer cell responses in the rat, it maps to the major histocompatibility complex (MHC) class I-like RT1C region, and it requires homozygous expression of RT1Cav1 alleles [3].
  • Immunological properties of subcellular rat lymphocyte preparations. Primary allogeneic stimulation in vitro by fractions containing Ia (RT1-B), but not RT1-A antigens [4].
  • In conjunction with previous breeding studies, this study maps the diabetes susceptibility gene to the right of the RT1-A locus and to the left of the RT1-C locus [5].
  • A cDNA clone encoding a RT1 E beta chain was isolated from a cDNA library prepared from Wistar (RT1 mu) spleen poly(A) RNA by screening with DNA fragments encoding a RT1 A beta chain [6].
  • LEW (RT1(1)) rats were primed for indirect T cell allorecognition of DA (RT1av1) classical class I MHC molecules by immunization with synthetic 22-24 amino acid peptides corresponding to the alpha-helices of the RT1-A class I molecule [7].

Biological context of RT1-A


Anatomical context of RT1-A

  • During mid and late pregnancy, RT1-A mainly localized in decidual blood vessels and spongiotrophoblast cells of the junction zone [12].
  • In late pregnancy, expression of RT1-A decreased in placenta and increased in uterus, and RT1-DM increased in both placenta and uterus with IFN-gamma treatment compared with untreated controls [12].
  • Immunohistochemical studies indicated that, in early pregnancy, RT1-DM protein mainly localized to luminal and glandular uterine epithelium, and RT1-A was present in deciduas basalis, outer layer of luminal epithelium and glandular epithelium [13].
  • Interestingly, after mechanical nerve injury, glial cells predominantely upregulated expression of RT1-A, whereas neuronal expression of RT1-U remained unchanged [14].
  • Individual rat cells producing antibody to rat MHC class I alloantigens ( RT1A ) and other erythrocyte (E)-associated alloantigens can be enumerated by a solid-phase antibody-forming cell focus ( AFCF ) assay [15].

Associations of RT1-A with chemical compounds


Regulatory relationships of RT1-A


Other interactions of RT1-A

  • Effect on expression of RT1-A and RT1-DM molecules of treatment with interferon-gamma at the maternal--fetal interface of pregnant rats [12].
  • Hence, it is possible to generate Ia-related allogeneic helper signals in primary, as well as secondary, in vitro responses, using subcellular membrane fragments that have restricted expression of RT1-B-, but not RT1-A-, encoded antigens [4].
  • The rats were classified into 5 groups according to the differences in subregions of the RT1 (rat MHC) between the recipient and the donor: group 1, RT1-A,B,D barrier (the differences of RT1-A,B,D subregions); group 2, RT1-A barrier; group 3, RT1-B,D barrier; group 4, RT1-B barrier; and group 5, RT1-D barrier [18].
  • Sequence analysis of the genomic interval between the Rps18 and RT1-A genes in the RT1u haplotype [19].

Analytical, diagnostic and therapeutic context of RT1-A


  1. Overexpression of neu-related lipocalin (NRL) in neu-initiated but not ras or chemically initiated rat mammary carcinomas. Stoesz, S.P., Gould, M.N. Oncogene (1995) [Pubmed]
  2. Susceptibility and resistance genes to insulin-dependent diabetes mellitus in the BB rat. Ono, S.J., Fuks, A., Guttmann, R.D., Colle, E. Exp. Clin. Immunogenet. (1989) [Pubmed]
  3. Generation of T cells with lytic specificity for atypical antigens. II. A novel antigen system in the rat dependent on homozygous expression of major histocompatibility complex genes of the class I-like RT1C region. Davies, J.D., Wilson, D.H., Butcher, G.W., Wilson, D.B. J. Exp. Med. (1991) [Pubmed]
  4. Immunological properties of subcellular rat lymphocyte preparations. Primary allogeneic stimulation in vitro by fractions containing Ia (RT1-B), but not RT1-A antigens. Kaldany, A., Carpenter, C.B., Shadur, C.A., George, K., Lundin, A.P., Suthanthiran, M., Strom, T.B. J. Exp. Med. (1980) [Pubmed]
  5. Association of susceptibility to spontaneous diabetes in rat with genes of major histocompatibility complex. Colle, E., Ono, S.J., Fuks, A., Guttmann, R.D., Seemayer, T.A. Diabetes (1988) [Pubmed]
  6. Complete structure of a rat RT1 E beta chain: extensive conservation of MHC class II beta chains. Robertson, K.A., McMaster, W.R. J. Immunol. (1985) [Pubmed]
  7. Indirect T cell allorecognition of donor antigens contributes to the rejection of vascularized kidney allografts. Benham, A.M., Sawyer, G.J., Fabre, J.W. Transplantation (1995) [Pubmed]
  8. Allorecognition of isolated, denatured chains of class I and class II major histocompatibility complex molecules. Evidence for an important role for indirect allorecognition in transplantation. Dalchau, R., Fangmann, J., Fabre, J.W. Eur. J. Immunol. (1992) [Pubmed]
  9. A detailed analysis of the potential of water-soluble classical class I MHC molecules for the suppression of kidney allograft rejection and in vitro cytotoxic T cell responses. Priestley, C.A., Dalchau, R., Sawyer, G.J., Fabre, J.W. Transplantation (1989) [Pubmed]
  10. The role of RT1 antigen differences in semi-allogeneic rat pregnancy. Power, D.A., Cunningham, C., Catto, G.R. Clin. Sci. (1987) [Pubmed]
  11. A single dose of the MHC-linked susceptibility determinant associated with the RT1u haplotype is permissive for insulin-dependent diabetes mellitus in the BB rat. Fuks, A., Ono, S.J., Colle, E., Guttmann, R.D. Exp. Clin. Immunogenet. (1990) [Pubmed]
  12. Effect on expression of RT1-A and RT1-DM molecules of treatment with interferon-gamma at the maternal--fetal interface of pregnant rats. Sun, Q.H., Peng, J.P., Xia, H.F., Yang, Y., Liu, M.L. Hum. Reprod. (2005) [Pubmed]
  13. Effects of IL-1 beta on RT1-A/RT1-DM at the maternal-fetal interface during pregnancy in rats. Xia, H.F., Peng, J.P., Sun, Q.H., Yang, Y., Liu, M.L. Front. Biosci. (2006) [Pubmed]
  14. Expression of nonclassical MHC class I (RT1-U) in certain neuronal populations of the central nervous system. Lidman, O., Olsson, T., Piehl, F. Eur. J. Neurosci. (1999) [Pubmed]
  15. Enumeration of rat allospecific antibody-producing cells by a solid-phase antibody-forming cell focus (AFCF) assay. Majoor, G.D. J. Immunol. Methods (1984) [Pubmed]
  16. Alloantibody and transferable suppressor activity induced by cyclosporine and blood transfusions in the rat. Jones, M.C., Power, D.A., Cunningham, C., Stewart, K.N., Catto, G.R. Transplantation (1988) [Pubmed]
  17. The effect of bile acids and piroxicam on MHC antigen expression in rat colonocytes during colon cancer development. Rigas, B., Tsioulias, G.J., Allan, C., Wali, R.K., Brasitus, T.A. Immunology (1994) [Pubmed]
  18. Effects of major histocompatibility complex matching on graft survival in allogeneic rat limb transplantation. Iwasaki, N., Gohda, T., Itoga, H., Minami, A., Kaneda, K. The Journal of hand surgery. (2001) [Pubmed]
  19. Sequence analysis of the genomic interval between the Rps18 and RT1-A genes in the RT1u haplotype. Walter, L., Günther, E. Transplant. Proc. (1999) [Pubmed]
  20. Immune mechanisms in organ allograft rejection. V. Pivotal role of the cytotoxic-suppressor T cell subset in the rejection of heart grafts bearing isolated class I disparities in the inbred rat. Lowry, R.P., Forbes, R.D., Blackburn, J.H., Marghesco, D.M. Transplantation (1985) [Pubmed]
  21. Morphologic studies of acute rat cardiac allograft rejection across an isolated major histocompatibility complex class I (RT1A) disparity. Forbes, R.D., Lowry, R.P., Darden, A.G., Gomersall, M., Marghesco, D.M. Transplantation (1988) [Pubmed]
  22. Changes in fecal fat excretion from allo-intestine transplanted rats after discontinuance of immunosuppressive agents. Saito, T., Kobayashi, E., Ogino, Y., Kaneko, K., Fujimura, A., Miyata, M. J. Gastroenterol. (1999) [Pubmed]
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