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Potentiation of a primary in vivo antibody response by alloantisera against gene products of the I region of the H-2 complex.

  • M Pierres
  • R N Germain
  • M E Dorf
  • B Benacerraf
Publication Date
Sep 01, 1977


Mice were immunized intravenously with suboptimal numbers (3.5-5 X 10(5)) of sheep erythrocytes together with various anti-Ia antisera or with sheep erythrocytes alone, and the primary IgM and IgG plaque-forming cell responses were assayed 6 days later9 A/J (H-2a) mice given 5 X 10(5) sheep erythrocytes together with as little as 0.4 mul of a (129 X A.TH)F1 anti-A.TL (anti-Iak) antiserum developed 2-3 times as many IgM and IGG plaque-forming cells as mice injected with antigen alone or together with various antisera not containing anti-Ia antibodies. Similar results were obtained with BALB/c (H-2d) mice and a (C3H X LG/Ckc)F1 anti-C3H. OH (anti-Iad) antiserum plus sheep erythrocytes. In the case of the anti-Iad antiserum, the potentiating activity could be absorbed with C3H. OH (Id) but not C3H(Ik) spleen cells, demonstrating that the active antibodies were specific for the Id region. Antiserum to I-Jk subregion-coded determinants was tested in A/J (I-Jk) mice and found to also potentiate 2- to 3-fold the plaque-forming cell response to suboptimal erythrocyte immunization. This antiserum [(BIO.A(3R) X DBA/2)F1 anti-B10.(5R)] failed to potentiate responses in BALB/c (I-Jd) mice, as expected on a genetic basis. The potentiating antibodies could be removed by absorption with B10.BR (I-Jk) but not B10 (I-Jb) spleen cells, also confirming the I-J specificity of the activity. The interference of anti-I-J antibodies with T lymphocyte suppressor mechanisms is prposed as a possible explanation for this phenomenon.

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