These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Immunological alterations inducible by mercury compounds. III. H-2A acts as an immune response and H-2E as an immune "suppression" locus for HgCl2-induced antinucleolar autoantibodies.
    Author: Mirtcheva J, Pfeiffer C, De Bruijn JA, Jacquesmart F, Gleichmann E.
    Journal: Eur J Immunol; 1989 Dec; 19(12):2257-61. PubMed ID: 2558021.
    Abstract:
    In responder mouse strains repeated injections of subtoxic doses of HgCl2 induce formation of antinuclear autoantibodies (ANA) and antinucleolar autoantibodies (ANolA). Others have shown that responsiveness to HgCl2-induced formation of ANA and ANolA is linked to H-2. Here, we extend these studies to a variety of mouse strains not tested previously. After confirming that strain B10.S (H-2s) is a high responder we have shown that strains B10.D2 (H-2d) and B10.BR (H-2k) are nonresponders. By comparing a panel of strains carrying appropriate intra-H-2 recombinant haplotypes derived from d, k and s, we were able to map responsiveness to As. Interestingly, among four strains all of which were As, and thus responsive, only the two H-2E- ones, B10.S and B10.RSD2, were high responders whereas the two H-2E+ ones, B10.HTT and B10.S(9R), were significantly less responsive. Thus, the genetics of HgCl2-induced autoantibody formation follow the rules established for immune responses to a variety of different antigens in that expression of H-2E "suppressed" the response.
    [Abstract] [Full Text] [Related] [New Search]