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Abstract

Directly stated, the function of the immune system is to eliminate intruding microorganisms or certain large molecules that enter the milieu of the body. Immunity is the successful outcome of this mechanism and its failure is progressive infection. Apart from the overt congenital or acquired immune deficiencies, there are also more subtle variations in the “resistance” of individuals to specific components of microorganisms that are under the control of alternative genes coding for functionally different molecules involved in immune recognition. There inherited elements are the “immune response genes,” and their study is “immunogenetics.”

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References

  • Babbitt, B., Allen, P., Matsueda, G., Haber, E., and Unanue, E., 1985, Binding of immunogenic peptides to la histocompatibility molecules, Nature 317:359–361.

    Article  PubMed  CAS  Google Scholar 

  • Bjorkman, P. J., Saper, M. A., Samraoui, B., Bennett, W. S., Strominger, J. L., and Wiley, D. C, 1987, Structure of the human class I histocompatibility antigen, HLA-A2, Nature 329:506–512.

    Article  PubMed  CAS  Google Scholar 

  • Bodmer, W. F., 1989, HLA 1987, in: lmmunobiology of HLA, Volume II: Immunogenetics and Histocompatibility (B. Dupont, ed.), Springer-Verlag, New York, p. 1.

    Google Scholar 

  • Buus, S., Sette, A., Colon, S. M., Jenis, D. M., and Grey, H. M., 1986, Isolation and characterization of antigen-la complexes involved in T cell recognition, Cell 47:1071–1077.

    Article  PubMed  CAS  Google Scholar 

  • Garrett, T. P. J., Saper, M. A., Bjorkman, P. J., Strominger, J. L., and Wiley, D. C, 1989, Specificity pockets for the side chains of peptide antigens in HLA-Aw68, Nature 342:692–696.

    Article  PubMed  CAS  Google Scholar 

  • Gregersen, P. K., Silver, J., and Winchester, R. J., 1987, The shared epitope hypothesis—an approach to understanding the molecular genetics of rheumatoid arthritis susceptibility, Arthritis Rheum. 30:1205–1213.

    Article  PubMed  CAS  Google Scholar 

  • Gregersen, P. K., Todd, J. A., Erlich, H. A., Long, E., Servenius, B., Choi, E., Kao, H. T., and Lee, J. S., 1989, First domain sequence diversity of DR and DQ subregion alleles, in: Immunobiology of HLA, Volume I: Histocompatibility Testing 1987 (B. Dupont, ed.), Springer-Verlag, New York, p. 1027.

    Google Scholar 

  • Kappler, J. W., Roehm, N., and Marrack, P., 1987, T cell tolerance by clonal elimination in the thymus, Cell 49:273–280.

    Article  PubMed  CAS  Google Scholar 

  • Kappler, J. W., Staerz, U., White, J., and Marrack, P. C, 1988, Self-tolerance eliminates T cells specific for Mis-modified products of the major histocompatibility complex, Nature 332:35–40.

    Article  PubMed  CAS  Google Scholar 

  • Kappler, J., Kotzin, B., Herron, L., Gelfand, E. W., Bigler, R. D, Boylston, A., Carrel, S., Posnett, D. N., Choi, Y, and Marrack, P., 1989, Vβ-specific stimulation of human T cells by staphylococcal toxins, Science 244:813.

    Article  Google Scholar 

  • Klein, J., 1982, Immunology, Wiley: New York.

    Google Scholar 

  • Nakamura, M., Burastero, S. E., Ueki, Y., Larrick, J. W., Notkins, A. L., and Casali, P., 1988, Probing the normal and autoimmune B cell repertoire with EBV High frequency of B cells producing monoreactive high affinity autoantibodies in patients with Hashimoto’s disease and SLE, J.Immunol 141:4160.

    Google Scholar 

  • Parham, P., Lawlor, D. A., Salter, R. D, Lomen, C. E., Bjorkman, P. J., and Ennis, P. D, 1989, HLA-A,B,C: Patterns of polymorphism in peptide-binding proteins, in: Immunobiology of HLA, Volume II: Immunogenetics and Histocompatibility (B. Dupont, ed), Springer-Verlag, New York, p. 10.

    Google Scholar 

  • Paul, W., 1984, in: Fundamental Immunology (W. Paul, ed.), Raven, New York, p. 439.

    Google Scholar 

  • Rosenthal, A. S., 1978, Determinant selection and macrophage function in genetic control of the immune response, Immunol. Rev. 40:136.

    Article  PubMed  CAS  Google Scholar 

  • Saito, T., Weiss, A., Miller, J., Norcross, M. A., and Germain, R. N., 1987, Specific antigen-la activation of transfected human T cells expressing murine Ti alpha beta-human T3 receptor complexes, Nature 325:125–130.

    Article  PubMed  CAS  Google Scholar 

  • Schaeffer, E. B., Sette, A., Johnson, D. L., Bekoff, M. C., Smith, J. A., Grey, H. M., and Buus, S., 1989, Relative contribution of “determinant selection” and “holes in the T-cell repertoire” to T-cell responses. Proc. Natl. Acad. Sci. USA 86:4649–4653.

    Article  PubMed  CAS  Google Scholar 

  • Steere, A. C., Dwyer, E., and Winchester, R., 1990, Association of chronic Lyme arthritis with HLA-DR4 and HLA-DR2 alleles, N. Engl. J. Med. 323:219–223.

    Article  PubMed  CAS  Google Scholar 

  • Vidovic, D., and Matzinger, P., 1988, Unresponsiveness to a foreign antigen can be caused by self-tolerance, Nature 336:222–225.

    Article  PubMed  CAS  Google Scholar 

  • Williams, A. F., and Barclay, A. N., 1988, The immunoglobulin superfamily—domains for cell surface recognition, Annu Rev. Immunol. 6:381–406.

    Article  PubMed  CAS  Google Scholar 

  • Winchester, R., 1990, Mapping susceptibility to rheumatoid arthritis into a conformationally equivalent region of MHC class II molecules encoded by different alleles, in: Molecular Aspects of Autoimmunity (N. R. Farid, ed.), Academic Press, Orlando, pp. 241–263.

    Google Scholar 

  • Winchester, R., and Dwyer, E., 1991, MHC and autoimmune diseases: Susceptibility to rheumatoid arthritis associated with a hydrophobic strip of a helix encoded by several MHC alleles, in: Molecular Immunobiology of Self Reactivity (C. A. Bona and A. Kaushik, eds.), Marcel Dekker, New York.

    Google Scholar 

  • Winchester, R., and Gregersen, P. K., 1988, The molecular basis of susceptibility to rheumatoid arthritis: The conformational equivalence hypothesis, Springer Semin. Immunopathol. 10:119–139.

    Article  PubMed  CAS  Google Scholar 

  • Winchester, R., and Kunkel, H. G., 1979, The human la system, Adv. Immunol. 28:221–292.

    Article  PubMed  CAS  Google Scholar 

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© 1992 Springer Science+Business Media New York

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Winchester, R. (1992). Human Immune Response Genes. In: Rugstad, H.E., Endresen, L., Førre, Ø. (eds) Immunopharmacology in Autoimmune Diseases and Transplantation. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1167-4_1

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  • DOI: https://doi.org/10.1007/978-1-4899-1167-4_1

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4899-1169-8

  • Online ISBN: 978-1-4899-1167-4

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