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Lymphotactin: a key regulator of lymphocyte trafficking during acute graft rejection
Author(s) -
J D Wang,
Norio omura,
Shiro Takahara,
B S Li,
Haruhito Azuma,
Naotsugu Ichimaru,
Yukito Kokado,
Kiyomi Matsumiya,
Tetsuzou Miki,
Seiichi Suzuki,
Äkïhïko Okuyama
Publication year - 1998
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1998.00570.x
Subject(s) - regulator , immunology , key (lock) , lymphocyte subsets , medicine , microbiology and biotechnology , biology , immune system , t cell , genetics , gene , ecology
The attraction of leucocytes to allografts is essential for rejection. The prcocess is controlled by chemokines. In order to clarify the role of lymphotactin (a cytokine that represents a novel branch of the chemokine superfamily) in regulating leucocyte trafficking during graft rejection, we used rat renal transplantation models to examine its gene expression and the distribution of lymphotactin‐expressing cells in renal grafts. Lymphotactin mRNA was upregulated strongly in acutely rejecting renal allografts. The mRNA was undetectable in isografts, chronically rejecting renal allografts or normal kidney. Once lymphotactin was expressed, large numbers of infiltrating lymphocytes were seen. Moreover extended studies demonstrated that in cultured rat spleen cells the expression of lymphotactin mRNA was markedly induced by phytohaemagglutinin (PHA) or phorbol myristate acetate (PMA), and such induction was inhibited by the immunosuppressive drugs FK506 and cyclosporin. Collectively, these observations provide new evidence demonstrating that lymphotactin is a key regulator of lymphocyte motility and adhesiveness during acute allograft rejection. FK506 and cyclosporin inhibition of lymphotactin expression is likely to represent an important molecular mechanism of the action of the drugs.

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