Immune responses during human Schistosomiasis mansoni. Evidence for antiidiotypic T lymphocyte responsiveness.

Abstract

We present a method for the examination of antiidiotypic cellmediated reactivity during chronic human infections. Pooled and individual sera from patients with schistosomiasis. mansoni were purified on immunoaffinity columns of schistosomal egg antigens (SEA). The eluates contained anti-SEA antibodies, but not SEA. These antibody preparations, and their F(ab')2 fragments, stimulated dose-dependent proliferation of peripheral blood mononuclear cells (PBMN) and T lymphocytes from some, but not all active or former schistosomiasis mansoni patients, and could do so autologously. Stimulation required presentation by plasticadherent cells. The eluates did not stimulate PBMN from persons who had never had schistosomiasis. Affinity-purified anti-SEA antibodies from former patients (cured for >10 yr) did not stimulate PBMN from patients with active infections. Reabsorption on SEA columns removed stimulatory activity from the eluates. We propose that multiclonal, SEA-related idiotypes expressed by some anti-SEA antibodies stimulate proliferation of T lymphocytes that express antiidiotypic specificities.

Cytokine Regulation of Human Immune Response to Schistosoma mansoni: Analysis of the Role of IL‐4, IL‐5 and IL‐10 on Peripheral Blood Mononuclear Cell Responses

“…Among the most well studied immune factors involved in immunoregulation are antibodies, which have been shown to act via idiotype/anti-idiotype interactions [5,6], adherent cells [7,8], 'suppressor cells' [9], immunocomplexes [10] and soluble factors [11]. A crucial role of T cells in the pathology of the infection has been demonstrated [12].…”

“…Although there are several immune components that have been correlated with regulation of the immune response in human schistosomiasis [5][6][7][8][9][10][11][12][13]21], little is known about the role of cytokines in the modulatory activity of the immune response during Schistosoma mansoni infection in man. In this paper we evaluate the role of IL-4, IL-5 and IL-10 on the proliferative PBMC responses of acute versus chronic patients (INT and HS) to SWAP and SEA.…”

Idiotypic sensitization in utero of children born to mothers with schistosomiasis or Chagas' disease.

“…We have used an in vitro proliferative assay to detect the presence of anti-Id T cells in the blood of patients with either or both schistosomiasis and Chagas' disease (15)(16)(17)(18)(19). In this system, the appropriate T cells proliferate in response to immunoaffinity-purified or monoclonal (20,21) antibodies, against Schistosoma mansoni-soluble egg antigens (SEA)' or T. cruzi epimastigote antigens (EPI) (15,17,18).…”

“…In this system, the appropriate T cells proliferate in response to immunoaffinity-purified or monoclonal (20,21) antibodies, against Schistosoma mansoni-soluble egg antigens (SEA)' or T. cruzi epimastigote antigens (EPI) (15,17,18). PBMC from individuals who have never had these infections are unresponsive to these antibodies, and neither patients with these infections nor uninfected subjects respond in culture to preparations of normal human immunoglobulin.…”

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.…”