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Limited usage of T‐Cell receptor β chains and sequences of the complementarity determining region 3 of lymphocytes infiltrating in the liver of autoimmune hepatitis
Author(s) -
Hoshino Yuji,
Enomoto Nobuyuki,
Izumi Namiki,
Kurosaki Masayuki,
Marumo Fumiaki,
Sato Chifumi
Publication year - 1995
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840220123
Subject(s) - t cell receptor , complementarity determining region , antigen , autoimmune hepatitis , biology , immunology , hepatitis , microbiology and biotechnology , t cell , immune system , antibody , immunoglobulin light chain
To study the role of antigen‐specific T lymphocytes in the pathogenesis of autoimmune hepatitis, messenger RNA of T‐cell receptors (TCR) was analyzed in liver biopsy specimens from four patients with autoimmune hepatitis. Using the TCR β‐chain variable region family specific oligonucleotides, a remarkable bias for the usage of β‐chain variable region 3 was detected in all four patients. Therefore, nucleotide and amino acid sequences of the complementarity‐determining region 3 rearranged to the β‐chain variable region 3, which is a putative contact site for peptide fragments from antigens bound in the groove of the human leukocyte antigen molecule, was further analyzed in randomly selected 10 clones from each patient. An Asp‐Arg‐Pro motif in the complementarity‐determining region 3 was identified in three of four patients with human leukocyte antigen DR4, and this motif was always rearranged to the β‐chain junctional region 1.2. From these results, β‐chain variable region 3 + , Asp‐Arg‐Pro + β‐chain junctional region 1.2 + T‐cell clones may be among the responsible lymphocytes involved in the liver damage in autoimmune hepatitis, especially in patients with human leukocyte antigen DR4. Thus, an analysis of the complementarity‐determining region 3 may give us an important clue to clarify characteristics of target antigens included in autoimmune hepatitis. (H EPATOLOGY 1995; 22:142–147.)