Abstract
We examined the effects of actarit, a new antirheumatic drug, on antibody production after LPS stimulation in mice. Actarit did not affect the proliferative response of B-cells stimulated with LPS or anti-mouse μ-chain antibody plus rIL-4. Lymphocytes in the Peyer's patches (PP) of mice with oral administration of actarit suppressed the production of IgA (not IgM and IgG) by B-cells stimulated with LPS. Actarit affected neither the serum level of IgA nor IgA secretion from the gut of mice without LPS stimulation. Actarit did not change the percentage of Thy-1 + cells in the PP lymphocyte population or that of CD4 + or CD8 + cells in the Thy-1 + fraction of PP lymphocytes. The suppressive effect of PP lymphocytes from mice treated with actarit was abrogated by the elimination of CD4 + cells (not CD8 + cells) from PP lymphocytes. These results suggest that actarit activates CD4 + suppressor T-cells in the PP, resulting in a specific suppression of IgA production after LPS stimulation.
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