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T cell activation by Theileria annulata ‐infected macrophages correlates with cytokine production
Author(s) -
BROWN D. J.,
CAMPBELL J. D. M.,
RUSSELL G. C.,
HOPKINS J.,
GLASS E. J.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb03845.x
Subject(s) - biology , clone (java method) , cytokine , t cell , microbiology and biotechnology , major histocompatibility complex , tumor necrosis factor alpha , immunology , immune system , gene , biochemistry
SUMMARY A major feature of the pathology induced by Theileria annulata is acute lymphocytic proliferation, and this study investigates the mechanisms underlying the intrinsic ability of T. annulata ‐infected monocytes to induce naive autologous T cells to proliferate. Different T. annulata ‐infected clones expressed different but constant levels of MHC class II, varying from < 1.0 × 10 5 to 1.5 × 10 6 molecules/cell, as measured by saturation binding. However, no correlation was found between the level of MHC class II expression and levels of induced T cell proliferation. Theileria anmulata infected cell lines and clones were assayed for cytokine mRNA expression by reverse transcriptionpolymerase chain reaction (RT‐PCR). The infected cells assayed produced mRNA specific forIL‐lα, IL‐1β, lL‐6, IL‐10 and tumour necrosis factor‐alpha (TNF‐a). but not IL‐2 or lL‐4. One clone (clone G)did not produce mRNA for TNF‐α. The degree of T cell proliferation induced by infected cells was directly correlated with the amount of mRNA produced for the T cell stimulatory cytokines IL‐lα and IL‐6, as assessed by a semiquantitative technique. In contrast, cells infected with the related parasite T. parva produced mRNA for IL‐lα, IL‐2, IL‐4, IL‐10 and interferon‐gamma (IFN‐γ). Since T. parva ‐infected cells also induce naive autologous T cell proliferation, it seems likely that the production of lL‐1α by cells infected with either parasite is a major signal for the induction of non‐specific T cell proliferation.

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