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Restricted use of T‐cell receptor V beta genes in posttransfusion graft‐ versus‐host disease
Author(s) -
Wang L.,
Tadokoro K.,
Tokunaga K.,
Uchida S.,
Moriyama S.,
Bannai M.,
Mitsunaga S.,
Takai K.,
Juji T.
Publication year - 1997
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1997.37111298088050.x
Subject(s) - immunology , biology , receptor , complementary dna , t cell , immune system , human leukocyte antigen , antigen , gene , microbiology and biotechnology , graft versus host disease , t cell receptor , beta (programming language) , t lymphocyte , genetics , stem cell , computer science , programming language
BACKGROUND: Posttransfusion graft‐versus‐host disease (PT‐GVHD) is a pathophysiological process of the immune system. Mature donor T cells that have survived the host defense mechanisms recognize recipient allo‐ antigens through antigen‐specific T‐cell receptors and mount an immune attack against certain host antigens. STUDY DESIGN AND METHODS: To characterize the T cells involved in PT‐GVHD, expression of the T‐cell receptor V beta genes in peripheral blood T cells isolated from four PT‐ GVHD patients was analyzed. T‐cell receptor beta chain cDNA derived from mRNA extracted from peripheral blood lymphocytes was amplified by an inverse polymerase chain reaction method, and the cDNA was subsequently cloned and sequenced. RESULTS: The cDNA clones derived from patients with PT‐GVHD showed remarkable differences in the distribution of T‐cell receptor V beta gene use from that in normal controls. Very restricted T‐cell receptor V beta gene repertoires and preferential expression of certain V beta gene segments were revealed in the peripheral blood lymphocytes of each patients. Shared V beta gene use among the patients was not observed, probably because of HLA differences among the patient‐donor combinations. CONCLUSION: This restricted use reflected in vivo expansion of a limited number of engrafted T‐cell clones at the onset of PT‐GVHD and suggested that those oligoclonal donor T cells may be involved in the induction of PT‐ GVHD.