Immune Responses during Human Schistosomiasis Mansoni

Abstract

T lymphocyte immunoregulatory subsets (T4+ and T8+ cells) have been analysed in eight cases of hepatosplenic schistosomiasis mansoni, and compared to parallel analyses of seven intestinal Schistosoma mansoni-infected patients and four uninfected control subjects. The mean T4+:T8+ ratio in hepatosplenic cases was markedly less than observed in other groups (0.94 vs 1.86 vs 2.22, respectively). Proliferative responses stimulated by a soluble adult worm extract correlated directly with the observed T4:T8 ratios. Normal levels of E rosette-positive and surface immunoglobulin-bearing lymphoid cells were observed in intestinal patients, while hepatosplenic patients demonstrated normal B lymphocyte proportions but highly erratic E rosette-positive percentages. Curiously, in hepatosplenic patients the percentage of E rosette-positive cells often did not correlate with the proportion of T3+ cells.

Early development and progression of lymphocyte‐stimulatory cross‐reactive idiotypes expressed on antibodies to soluble egg antigens during Schistosoma mansoni infection of mice

“…In both the current and former studies [12], Id preparations that stimulated the highest level of anti-Id proliferation temporally preceded the presence of anti-Id spleen cells that responded best to those Id. The progressively decreased levels of proliferation observed upon exposure of spleen cells from infected mice to 7WkId, 8WkId, 12WkId, or 16WkId may again reflect some dilution of a given set of anti-SEA Ab that express stimulatory CRI during a period of rapidly increasing Ab responsiveness [5].…”

“…However, we are unaware of data that address the relative ability of IgM, IgG, or IgA Id-bearing Ab of identical Ag specificity and Id representation to stimulate anti-Id T cell proliferation, and production of preparations of such Ig molecules would be difficult to achieve. Interestingly, 6WkId had the highest level of anti-SEA IgG2a, an isotype subclass associated with T h l cell-mediated immune responses [18] at the very beginning of responses against eggs, which are known ultimately to engender Th2-type responsiveness [ 19, 201. Ab responses measurable against S. mansoni SEA in mice have been shown to increase during the acute phase to reach peak levels in circulation concordant with, or after, the onset of spontaneous modulation of granuloma formation [ 5 ] . Peak levels of anti-SEA CRI in mice have been detected in this and other studies [12] early in the infection at the time of maximum anti-SEA cellular responsiveness, prior to onset of immunomodulation of granuloma formation [5].…”

“…Interestingly, 6WkId had the highest level of anti-SEA IgG2a, an isotype subclass associated with T h l cell-mediated immune responses [18] at the very beginning of responses against eggs, which are known ultimately to engender Th2-type responsiveness [ 19, 201. Ab responses measurable against S. mansoni SEA in mice have been shown to increase during the acute phase to reach peak levels in circulation concordant with, or after, the onset of spontaneous modulation of granuloma formation [ 5 ] . Peak levels of anti-SEA CRI in mice have been detected in this and other studies [12] early in the infection at the time of maximum anti-SEA cellular responsiveness, prior to onset of immunomodulation of granuloma formation [5]. The fact that these CRI on anti-SEA Ah from mice infected for 8 weeks cross-react serologically with Id from schistosomiasis patients with chronic asymptomatic disease [12] is consistent with the hypothesis that these CRIbearing antibodies may play a role in the immunopathogenesis of schistosomiasis in mice.…”

Systemic modulation of peripheral eosinophilia (air pouch model) in Schistosoma mansoni infection

“…In the pre-oviposition phase of the infection occurred an up-modulation, while in the acute (7 weeks) and chronic (14 weeks) phases, the eosinophil response was down-modulated. The literature has emphasized multiple putative immunoregulatory mechanisms, during the course of S. mansoni infection, such as suppressor T cell activity (Colley et al 1978), adherent phagocytic suppressor cells (Todd et al 1979), serum-mediated suppression (Colley et al 1977, Ottesen & Poindexter 1980, circulating immune complexes ) and idiotypic/anti-idiotypic interactions, involving also anti-idiotypic T lymphocytes (Lima et al 1986, Powell & Colley 1987, Parra et al 1988, 1991. However, all these mechanisms are related to the pos-oviposition phases of the infection, and probably some of them interfere with eosinophil response.…”