Immune Mechanisms in Chlamydial Eye Infection: Cellular Immune Responses In Chronic and Acute Disease

Abstract

The current studies detail cell-mediated immune responses to Chlamydia trachomatis antigen in both acute and chronically infected monkeys. Peripheral blood mononuclear leukocytes (PBMLs) from three groups of animals (immunized before infection, not immunized before infection, and chronically infected) were tested for the capacity to proliferate in response to C. trachomatis antigen in vitro. Only those animals that had been systemically immunized before acute ocular infection responded significantly. Coculturing macrophages from nonresponding animals with T cells from D-histocompatible responding animals showed that the ability to present antigen was unaffected in nonresponding animals. These studies also demonstrated that removal of suppressor T cells from PBMLs before culture resulted in increased proliferation in the chronically infected group and suggested that the nonresponsiveness seen in chronic ocular disease may be mediated by suppressor T cells.

Lymphocyte proliferative responses to chlamydial antigens in human chlamydial eye infections

“…Thus the higher score in the vaccinated group may in fact indicate that there was less scarring in this group, and hence a more rather than a less favourable outcome. Young & Taylor (1984) found lymphocyte proliferative responses to chlamydial antigens to be suppressed after repeated reinfection of cynomolgus monkeys, apparently due to the activation of specific CD8+ suppressor T cells. They postulated that such suppressor mechanisms might play a part in the persistence of chlamydial infection in trachoma endemic areas.…”

A Survey of Trachoma: The Histopathology and the Mechanism of Progressive Cicatrization of Eyelid Tissues

“…It is interesting to note that only small numbers of macrophages were seen and these were not associated with follicles. In some granulomatous disease states, schistosomiasis for example, monokines have been strongly implicated in the induction of fibrosis [4, 9]. …”

“…The immune response seems to confer partial protection against subsequent infection, yet appears also to be responsible for much of the observed pathology and tissue destruction seen in trachoma [4, 5, 6]. Interesting findings in areas of C. trachomatis pathogenesis further delineate the complex bacteria-host relationship in disease and may have implications for vaccine design.…”

Conjunctival lymphocyte subsets in trachoma

“…It is suspected that imbalances or defects in the immunoregulatory system may contribute to the entire disease process in chlamydial infections. In a cicatrizing trachoma model in cynomolgus monkeys it has been shown that repeated ocular inoculation of Chlamydia trachomatis resulted in activation without increase in numbers of peripheral blood T-suppressor lymphocytes which decreased the normal proliferation of lymphocytes to Chlamydia trachomatis [8]. In a recent study which evaluated the lymphoid populations present in the lymphoid follicles of experimentally induced trachoma in monkeys it was found that there was an increase in the numbers of both T-helper and Tsuppressor/cytotoxic lymphocytes during the peak conjunctival inflammatory response, however, T-E.M. Burd, K.F.…”

“…It is not known whether the lymphocytes staining with OKT8 are T-suppressor or T-cytotoxic lymphocytes. If they are T-suppressor lymphocytes, the mechanism present locally may be similar to that seen systemically [8] in that the influx of T-suppressor lymphocytes may inhibit the proliferative response to chlamydial antigen and result in persistence of infection. Monocytes which infiltrate in response to the persistent infection may secrete factors such as interleukin-1 or fibroblast activating factors which trigger proliferation of scar tissue [7].…”