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The anthelmintic drug praziquantel promotes human Tr1 differentiation
Author(s) -
Eyoh Enwono,
McCallum Patrick,
Killick Justin,
Amanfo Seth,
Mutapi Francisca,
Astier Anne L
Publication year - 2019
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.12229
Subject(s) - praziquantel , immune system , anthelmintic , biology , immunology , t cell , secretion , antigen , microbiology and biotechnology , pharmacology , helminths , schistosomiasis , endocrinology , ecology
Abstract Praziquantel ( PZQ ) is an anthelminthic human and veterinary drug used to treat trematode and cestode worms. Changes in immune responses have been demonstrated in humans following curative PZQ treatment of schistosome infections. These changes have been attributed to the removal of immunosupressive worms and immune responses to parasite antigens exposed from dying worms. To date, there has been no study investigating the potential direct effect of PZQ on the host immune cells. Herein, we analyzed the effect of PZQ on human CD 4 + T cells classically costimulated by CD 3/ CD 28 or costimulated by the complement regulator CD 46 to induce Type 1 regulatory T cells (Tr1). Our results show that PZQ enhanced T‐cell proliferation, increased secretion of IL ‐17 and IL ‐10 but had no effect on secretion of GM ‐ CSF or IFN γ. Moreover, PZQ increased the coexpression of CD 49b and LAG ‐3, a hallmark of Tr1 cells, suggesting increased Tr1 differentiation. Indeed, supernatants from PZQ ‐treated cells were able to decrease bystander T‐cell activation, and this was partly reduced when blocking IL ‐10. Hence, our study demonstrates that PZQ directly modulates human T‐cell activation and promotes Tr1 differentiation, suggesting that PZQ may have immunomodulatory functions in parasite‐unrelated human inflammatory diseases.