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Cytokines inhibit the development of trophozoite‐infected cells of Theileria annulata and Theileria parva but enhance the proliferation of macroschizont‐infected cell lines
Author(s) -
PRESTON PATRICIA M.,
BROWN C.G.D.,
RICHARDSON WENDY
Publication year - 1992
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1992.tb00456.x
Subject(s) - biology , theileria parva , theileria , virology , immunology , cell culture , cell growth , east coast fever , in vitro , parasite hosting , genetics , world wide web , computer science
Summary The following bovine (Bo) and human (Hu) cytokines—Bo rTNF‐a, Bo rIFN‐g, Hu IFN‐a, Hu rIL‐1, Hu rIL‐2—significantly inhibited the in vitro development of trophozoite‐infected cells of three stocks of Theileria annulata and of Theileria parva (Muguga). However, none of these cytokines inhibited the proliferation of established T. annulata or T. parva macroschizont‐infected cell lines. Indeed, Bo rTNF‐a and Hu rIL‐2 consistently enhanced the proliferation of macroschizont‐infected cell lines of both species and the blastogenesis of uninfected lymphocytes in trophozoite‐infected cultures. These results suggest that cytokines could help in resistance to challenge infections by preventing the further development of trophozoite‐infected cells but provide no evidence that any of the above cytokines directly help to resolve primary infections by inhibiting the growth of macroschizont‐infected cells. These findings also suggest that both TNF‐a and IL‐2 could play a role in the pathogenesis of Theileria infections by promoting the proliferation of macroschizont‐infected cells and the associated lymphoid hyperplasia.