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Recovery from Anti-Ig Induced Immunosuppression: Implications for a Model of Ig-Secreting Cell Development¹

Immunobiology Unit, Department of Microbiology, Montana State University, Bozeman, Montana 59715

Abstract

Data are presented on Ig levels in anti-Ig-treated BALB/c, congenitally athymic (nude) and littermate mice bled at intervals both during and after suppressive treatment. The patterns of suppression and recovery indicate that anti-µ antiserum is a powerful, but dose dependent, panspecific suppressor of humoral immunoglobulins, capable of permanent suppression of IgM in all mice but often allowing slow, partial recovery of other Ig classes. Anti- and anti- antisera are class-specific in their suppressive effect, but are of high efficacy and lasting effect only in the immunologically defective nude mouse. It is particularly noteworthy that anti- antiserum has no effect on IgA levels, even in nude mice.

From these data, a model for the development of Ig-producing cells has been developed. This model postulates that the precursors of cells producing all classes of Ig bear IgM receptors, but that these IgM-bearing cells represent early stages of four separate cell lines differentiating toward the production of IgM, IgG1, IgG2, and IgA, respectively. During this differentiation process, each line replaces, or at least supplements, these early IgM receptors with either IgM, IgG1, IgG2, or IgA receptors. Each of the resulting four cell lines is capable of producing a single class or subclass of antibody upon antigenic stimulation. It is further postulated that the panspecific suppressive effect of anti-µ treatment is achieved by arrest of this differentiation process, whereas the class-specific suppression resulting from anti- or anti- treatment is due to blocking of IgG or IgA receptors acquired during differentiation.

Footnotes

¹ This work was supported in part by United States Public Health Service Grants AI 06552-08, CA 15322-01, and AI 11625-01.

² National Institutes of Health Postdoctoral Fellow No. AI 55024-02.