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Human eosinophils modulate peripheral blood mononuclear cell response to Schistosoma mansoni adult worm antigen in vitro.

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Tweyongyere, R 
Namanya, H 
Naniima, P 
Cose, S 
Tukahebwa, EM 


High numbers of eosinophils are observed in parasitic infections and allergic diseases, where they are proposed to be terminally differentiated effector cells that play beneficial role in host defence, or cause harmful inflammatory response. Eosinophils have been associated with killing of schistosomulae in vitro, but there is growing evidence that eosinophils can play additional immuno-regulatory role. Here, we report results of a study that examines peripheral blood mononuclear cell (PBMC) cytokine responses to Schistosoma mansoni adult worm antigen (SWA) when stimulated alone or enriched with autologous eosinophils. Production of the Th-2 type cytokines interleukin (IL)-4, IL-5 and IL-13 was lower (P = 0·017, 0·018 and <0·001, respectively) in PBMC + eosinophil cultures than in PBMC-only cultures stimulated with SWA. Substantial levels of IL-13, IL-10, interferon gamma and tumour necrosis factor alpha were recorded in cultures of eosinophils, but none of these cytokines showed significant association with the observed eosinophil-induced drop in cytokine responses of PBMC. Transwell experiments suggested that the observed effect is due to soluble mediators that downmodulate production of Th-2 type cytokines. This study shows that eosinophils may down-modulate schistosome-specific Th-2 type cytokine responses in S. mansoni-infected individuals. The mechanism of this immune modulation remains to be elucidated.



cytokines, eosinophils, immune modulation, schistosomiasis, Adult, Animals, Antigens, Helminth, Cells, Cultured, Eosinophils, Humans, Interferon-gamma, Interleukin-10, Interleukin-13, Interleukin-4, Interleukin-5, Leukocytes, Mononuclear, Schistosoma mansoni, Schistosomiasis mansoni, Tumor Necrosis Factor-alpha

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Parasite Immunology

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Medical Research Council (G7708609)
Medical Research Council (MR/M019780/1)
Wellcome Trust (100891/Z/13/Z)
The study was a fellowship funded by Wellcome Trust, Makerere-UVRI Research Training Programme in Infection and Immunity (grant number 084344) and European Foundations Initiative for NTDs ‘EFINTD’ (grant ref 86 529). The study was carried out under co-infection studies programme lead by AME funded by Wellcome Trust (grant number 095778).