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Infect Immun. 1990 January; 58(1): 228-236

Immunosuppressive properties of the Mycoplasma arthritidis T-cell mitogen in vivo: inhibition of proliferative responses to T-cell mitogens.

Department of Internal Medicine, College of Medicine, University of Utah, Salt Lake City 84132.

ABSTRACT

We have previously shown that Mycoplasma arthritidis produces a soluble T-cell mitogen (MAM) which is active for most mouse strains that express the alpha chain of the I-E molecule (E alpha) encoded within the murine major histocompatibility complex. The lymphocytes from mice injected intravenously with the MAM exhibited a marked decrease in their ability to respond in vitro to MAM, to phytohemagglutinin, or to concanavalin A T-cell mitogens. Suppression could only be induced in MAM-responsive mouse strains and was most marked 1 to 4 days postinjection. Splenic and node cells and, to a lesser extent, thymic cells from MAM-injected mice could inhibit the ability of lymphocytes from normal mice to respond to MAM and lectin mitogens. A minimum of 2.5 x 10(4) viable cells was required for significant transfer of suppression, and no major histocompatibility complex restrictions were seen. Unlike concanavalin A-induced suppressor cells, which consist of a CD4-, CD8+ T-cell subset, suppressor cells induced by MAM were due to a CD4+ CD8- subset. We hypothesize that MAM may play a role in M. arthritidis-mediated disease by both its inflammatory and immunosuppressive properties.

This article has been cited by other articles:

• Mu, H.-H., Sawitzke, A. D., Cole, B. C. (2000). Modulation of Cytokine Profiles by the Mycoplasma Superantigen Mycoplasma arthritidis Mitogen Parallels Susceptibility to Arthritis Induced by M. arthritidis. Infect. Immun. 68: 1142-1149 [Abstract] [Full Text]