Advertisement

Biochemical Evidence for Multiple Ia Molecules

  • Chella S. David
  • William P. Lafuse
  • Michele Pierres
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 155)

Abstract

Both Ia antigens and Ir genes map to the I-A and I-E subregions of the mouse H-2 gene complex. The I-A subregion codes genes for three polypeptide chains, designated Aα, Aβ, and Eβ while the I-E subregion maps the gene for Eα (1). The map position of a third invariant Ia polypeptide chain designated I is not known. Thus, the I-A molecule and I-E molecule are formed by the non-covalent binding of the three chains, α (34,000 M.W.), β (28,000 M.W.) and I (31,000 M.W.). Recent studies using mutant strains and monoclonal antibodies have clearly shown that Ia antigens are the immune response gene products. The Ia molecules are involved in generating histo-incompatibility, alloreactivity, autoreactivity, as well as generating immune response to a variety of foreign antigens. Studies using alloreactive and antigen-specific T-cell clones have shown that Ia molecules most probably mediate immune activity by presentation of antigens to T-cells (2). Yet, it is not clear how the Ia molecules interact specifically with a variety of antigens under Ir gene control. One possibility is that Ia molecules have several antigenic sites which interact with different antigens. Recent studies have shown that there may be multiple epitopes of similar Ia antigens which are spatially distributed through the Ia molecule (3). Another possibility is that there are multiple Ia molecules, each of which can interact specifically with different antigens. To investigate this question, we have begun the biochemical study of Ia molecules using monoclonal antibodies. In this report, we will present preliminary evidence that there are multiple I-A and I-E molecules (4).

Keywords

Polypeptide Chain Alpha Chain Beta Chain Neuraminic Acid Adherent Cell Population 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Jones, P. P., Murphy, D. B., McDevitt, H. O., J. Exp. Med. 148:925, 1978.PubMedCrossRefGoogle Scholar
  2. 2.
    Fathman, C. G., Kimoto, M., Melvold, R. W., David, C. S., Proc. Natl. Acad. Sci. USA 78:1853, 1981.PubMedCrossRefGoogle Scholar
  3. 3.
    Pierres, M., Kourilsky, F. M., Rebovan, J. P., Dosseto, M., Caillol, D., Eur. J. Immunol. 10:950, 1980.PubMedCrossRefGoogle Scholar
  4. 4.
    Lafuse, W. P., Corser, P. S., David, C. S., Immunogenetics, in press.Google Scholar
  5. 5.
    Cullen, S. E., Kindle, C. S., Schreffler, D. C., Cowing, C., J. Immunol. 127:1478, 1981.PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • Chella S. David
    • 1
    • 2
  • William P. Lafuse
    • 1
    • 2
  • Michele Pierres
    • 1
    • 2
  1. 1.Department of ImmunologyMayo Clinic and Medical SchoolRochesterUSA
  2. 2.Centre d’ Immunologie InsermMarseilleFrance

Personalised recommendations