Fcϵ receptor‐positive cells are a major source of antigen‐induced interIeukin‐4 in spleens of mice infected with Schistosoma mansoni
When cultured in vitro with either mitogen or parasite antigens, spleen cells from mice infected with Schistosoma mansoni produce significantly higher levels of IL‐4 than splenocytes from control animals. Previous studies suggested that this increase in IL‐4 production occurs because of a selective...
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Veröffentlicht in: | European journal of immunology 1993-08, Vol.23 (8), p.1910-1916 |
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Zusammenfassung: | When cultured in vitro with either mitogen or parasite antigens, spleen cells from mice infected with Schistosoma mansoni produce significantly higher levels of IL‐4 than splenocytes from control animals. Previous studies suggested that this increase in IL‐4 production occurs because of a selective expansion of T helper type 2 (Th2) cells in infected mice. However, these experiments employed unfractionated spleen populations rather than purified T lymphocytes. Here we demonstrate that T‐depleted spleen cells from infected animals synthesize high levels of interleukin‐4 (IL‐4), but no IL‐5 when stimulated with parasite antigen in vitro. Nevertheless, when purified by sorting, T cells and non‐B, non‐T (NBNT) populations produced similar amounts of IL‐4 in response to parasite antigen. The IL‐4 producing NBNT cells were found to belong to an Fee receptor (FceR)‐positive population which after sort purification produced high levels of IL‐4 (between 1000 and 2000 U of per 5 × 103 cells). FACS analysis revealed that these FceR+ cells make up 0.53% of splenic NBNT cells in control animals while in 8‐9‐week‐infected animals they increase to 3.8% of that population. In contrast, in mice with 8‐week unisexual worm infections these cells comprise only 1.71% of NBNT cells, indicating that eggs are a major stimulus of the response. The expansion of FceR+ cells and their production of IL‐4 could be an important factor regulating the selection and induction of different CD4+ subsets in schistosome‐infected hosts. |
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ISSN: | 0014-2980 1521-4141 |
DOI: | 10.1002/eji.1830230827 |