Deficit of interleukin 2 production associated with impaired T-cell proliferative responses in Mycobacterium lepraemurium infection

Abstract

C57BL/6 and BALB/c mice were infected intravenously with 10(7) Mycobacterium lepraemurium (MLM). At various times after infection, spleen cells were tested for their capacity to proliferate in vitro in response to concanavalin A (ConA) and to allogeneic cells. The generation of alloreactive cytotoxic T lymphocytes was also studied. The mitogen- and allogeneic-cell-induced blastogenesis of splenocytes from MLM-infected C57BL/6 and BALB/c mice was shown to be depressed during infection. The maximal decrease occurred 6 months after infection. Conversely, no reduction in the ability to generate alloreactive cytotoxic T lymphocytes was observed even after 6 months of infection. At the same time, interleukin 2 (IL2) activity generated by ConA stimulation of infected splenocytes was measured in both strains. IL2 activity in the ConA-stimulated culture supernatants was decreased as early as 1 month after MLM inoculation as compared with supernatants from age-matched control mice. Thus, IL2 production by infected-mouse spleen cells was shown to decline earlier than their proliferative responses to ConA and to allogeneic cells. ConA-induced T-cell blasts from infected mice showed a reduced ability to proliferate when incubated with an IL2-containing reference supernatant from ConA-stimulated normal spleen cells. These data suggest that a defect in IL2 production and utilization might contribute to the impairment of T cell-mediated immunity observed in MLM-infected mice.

Defective interleukin 2 production and responsiveness in human pulmonary tuberculosis.

“…Responses to streptococcal antigen, however, were comparable to those of healthy donors. Deficient IL-2 production has been reported in a number of experimental settings (23)(24)(25). In humans, depressed IL-2 production has been shown in patients with the acquired immunodeficiency syndrome (26), lepromatous leprosy (27), and recurrent oral herpes simplex virus infection (28).…”

Immunologic dysfunction in the pathogenesis of periodontal diseases*

“…Such modulation of the immune response may be a critical event in the outcome of numerous infections including measles (Arneborn & Biberfeid 1983). rubella (Kauffman et al 1974, Olson et al 1968), influenza (Kantzler et al 1974), leprosy (Hoffenbach et al 1983. Mehra et al 1982, Bullock et al 1978, candidiasis (Carrow & Domer 1985, Rivas & Rogers 1983, leishmaniasis (Reiner & Finke 1983.…”

Inhibition of mitogen-induced proliferation of spleen lymphocytes is correlated with the induction of cell-mediated immunity in Salmonella infection in mice

“…Our results show that immunization with both viable cells and sonicate of S. typhimurium suppresses PHA-or ConA-induced proliferation of murine T-lymphocytes, but that the sonicate of E. coli K-12 does not. The reason for the occurrence of this type of T-cell suppression has been explained by the release of prostaglandin E from macrophages observed during Trypanosoma infection [14], or the decrease in IL-2 production during Mycobacterium lepraemurium infection [15], but the T-cell suppression induced by immunization with Salmonella in this study could not be reversed by the addition of indomethacin 1 h after stimulation with a mitogen. Also, since the levels of IL-2 secretion were almost the same in each immunized mouse, this did not explain the suppression of T-cell proliferation in our study (data not shown).…”