The Influence of I‐E on the Generation of Autoantibody and Specific Suppression in Rat Erythrocyte‐Immunized Mice

Abstract

A proportion of the antibodies produced by mice in response to the injection of rat erythrocytes (RRBC) cross-react with autologous red cells. When spleen cells from mice so immunized are transferred to naive syngeneic recipients, the recipient mice produce high anti-RRBC antibody titres but little or no autoantibody. This phenomenon has been attributed to the action of suppressor T cells. To date, the only mouse strain which consistently fails to demonstrate specific suppression of the autoantibody response is the SJL, which lacks the I-E molecules suggested to be important in the generation of suppressor T cells. The results presented here show that some, but not all, I-E negative strains of mice are capable of exhibiting transferable suppression of RRBC-induced antibodies.

Spontaneous Downregulation of Antibody/Autoantibody Synthesis in Susceptible Mice upon Chronic Exposure to Mercuric Chloride is not Owing to a General Immunosuppression

“…These results are in accordance with and confirm the general concept that in both susceptible rats and mice, mercury‐induced antibody/autoantibody responses are negatively controlled [6, 16–21, 29]. The exception that IgG1 ANolAs were constantly produced in SJL (H‐2 s ) mice, despite downregulation of other IgG1 autoantibody responses, is possibly owing to the presence of an unusual defect in the induction of suppression in certain specific autoantibody responses (including ANolA) in this strain [30]. Obviously, further studies are required to clarify this issue.…”

The Effect of Toxicokinetics on Murine Mercury-Induced Autoimmunity

“…The expression on the cell surface of the proteins encoded by this locus is defective in many of the strains with susceptible genes in the H-2A locus, and nonexpression of the H-2E proteins is associated with higher ANoA titer (Mirtcheva et al, 1989) and more extensive systemic IC deposits (Hultman et al, 1992). The dampening effect of the H-2E expression has been attributed to immunological mechanisms (Elliot and Cooke, 1992). Comparing the ANoA response to 5 mg Hg/L drinking water in the strains B10.S and B10.S(9R), both H-2AQ but only the latter expressing H-2E revealed a tendency to fewer ANoA-positive mice and a lower ANoA titer in the B10.S(9R) strain, although the differences were not significant.…”