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G1/S cell cycle arrest provoked in human T cells by antibody to CD26
Author(s) -
Ohnuma Kei,
Ishii Tomonori,
Iwata Satoshi,
Hosono Osamu,
Kawasaki Hiroshi,
Uchiyama Masahiko,
Tanaka Hirotoshi,
Yamochi Tadanori,
Dang Nam H.,
Morimoto Chikao
Publication year - 2002
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.1365-2567.2002.01510.x
Subject(s) - jurkat cells , t cell , dipeptidyl peptidase , monoclonal antibody , extracellular , dipeptidyl peptidase 4 , biology , transfection , microbiology and biotechnology , mapk/erk pathway , cell growth , cd28 , cell culture , antibody , kinase , enzyme , immunology , immune system , biochemistry , endocrinology , genetics , diabetes mellitus , type 2 diabetes
Summary CD26 is T cell costimulatory molecule with dipeptidyl peptidase IV (DPPIV) enzyme activity located in its extracellular region. The expression of CD26 is enhanced after activation of T cells, while it is preferentially expressed on a subset of CD4 + memory T cells in the resting state. In this paper, we demonstrate that binding of the soluble anti‐CD26 monoclonal antibody (mAb) 1F7 inhibits human T‐cell growth and proliferation in both CD26‐transfected Jurkat T‐cell lines and human T‐cell clones by inducing G1/S arrest, which is associated with enhancement of p21 Cip1 expression. This effect depends on the DPPIV enzyme activity of the CD26 molecule. Moreover, we show that expression of p21 Cip1 after treatment with the anti‐CD26 mAb 1F7 appears to be induced through activation of extracellular signal‐regulated kinase (ERK) pathway. These data thus suggest that anti‐CD26 treatment may have potential use in the clinical setting involving activated T cell dysregulation, including autoimmune disorders and graft‐vs.‐host disease.