Immunosuppression in trypanosomiasis: some thymus dependent and thymus independent responses

Biologically active products from African Trypanosomes.

“…Perhaps the most significant of all the immunological lesions which occur in the trypanosomiases is a profound immunosuppression. This immunosuppression, which involves both the antibody-mediated (51,54,75,76,84,98,181) and the cell-mediated (63,97,112) immune systems may be the most important pathogenic mechanism in these diseases. Because of this immunosuppression, it is common for trypanosome-infected individuals, both human and animal, to succumb not directly to the trypanosomes but to secondary infections and die as a result of pneumonias, sepsis, enteritis, or virus infections (4, 100).…”

Altered immune responsiveness associated with Encephalitozoon cuniculi infection in rabbits

“…abortus associated with E. cuniculi infection observed in this study has some precedent in studies on other parasitic diseases where an increase in largely nonspecific IgM has been noted (17). However, Murray et al (16) reported an absence of anti-sheep erythrocyte IgM in Trypanosoma brucei-infected mice 5 days after immunization, and Longstaffe et al (12), in similar experiments, found a decrease in IgM plaque-forming cells in T. brucei-infected, immunized mice.…”

Immunosuppression in Experimental African Trypanosomiasis

“…Indeed, a number of B-cell mitogens completely suppress prima ry immune responses in vitro to SRBC [9]. It is also possible that a loss of T-helper cell function would lead to B-cell unresponsi veness for T-dependent antigens [13,21,24,25], as well as the inability to 'switch' from IgM synthesis to IgG synthesis in mi togen-expanded B-cell clones [24], We have also recently suggested that the sustained hypocomplementemia in trypanosomiasis may also promote these immunological ab normalities [2,13].…”

“…Another characteristic of African trypan osome infections is the occurrence of large increases in the level of immunoglobulins in the circulation, particularly IgM [15,16,21,24,26,30]. In mice and rats infected with T. brucei, Hudson et al [16] and Mur ray et al [30] reported a rapid rise in back ground IgM PFC early in infection, fol lowed by a severe depression of antibody responses to antigens not related to the try panosome infection.…”

“…However, the paradox of the simultaneous association of a highly active immunological and mononuclear phagocytic system in trypanosomiasis [31,32] with an immunosuppressed state to other antigens [16,30] has greatly contributed to the diffi culty in the elucidation of this phenomenon. Nevertheless, the suggestion that B-cells, capable of recognizing the introduced anti gen, may be depleted as a result of poly clonal B-cell activation by trypanosomederived B-cell mitogens [1,2,10,14,16,30,40] has been supported by the observation of a rapid rise in background IgM plaque-form ing cells (PFC) early in infection [7,16], followed by severe depression of antibody responses to antigens not related to the try panosome infection [7,16,21,30]. This hy pothesis has also been supported by the demonstration that trypanosomes may be mitogenic in vitro [1,2,6,7,10,24], In this paper, studies on the nature of the trypanosome-derived factors which produce the mitogenic effect in vitro, and of the anti body responses to various antigens not re lated to the trypanosome during Trypanoso ma congolense infection, are reported.…”