Host intestinal intraepithelial γδ T lymphocytes present during acute graft‐versus‐host disease in mice may contribute to the development of enteropathy

Tetsu Sakai, Kyoko Ohara‐Inagaki, Toyonori Tsuzuki, Yasunobu Yoshikai

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    Abstract

    We reported that T cell receptor (TcR) γδ intestinal intraepithelial lymphocytes (i‐IEL) of host origin increased transiently, then decreased drastically at the early stage of non‐irradiated acute graft‐versus‐host disease (GVHD) in mice. We investigated the role of the TcR γδ i‐IEL of host origin in the pathogenesis of the intestinal lesions that occur during acute GVHD. The acute GVHD was induced in mice which had been depleted of TcR γδ by in vivo administration of hamster monoclonal antibody (mAb) against TcR γδ. Although the degree of splenomegaly after the induction of acute GVHD in mice treated with anti‐TcR γδ mAb was similar to that in control mice treated with hamster anti‐2,4,6‐trinitrophenyl mAb, infiltration of donor‐derived T cells into the epithelium, and mitosis and apoptosis of crypt cells in the intestinal mucosa were dramatically suppressed in these mice. This suggest that host TcR γδ T cells in i‐IEL contribute to the development of enteropathy in acute GVHD in mice.

    Original languageEnglish
    Pages (from-to)87-91
    Number of pages5
    JournalEuropean Journal of Immunology
    Volume25
    Issue number1
    DOIs
    Publication statusPublished - Jan 1 1995

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    Acute Disease
    T-Cell Antigen Receptor
    T-Lymphocytes
    Monoclonal Antibodies
    Lymphocytes
    Cricetinae
    Splenomegaly
    Intestinal Mucosa
    Mitosis
    Epithelium
    Apoptosis

    All Science Journal Classification (ASJC) codes

    • Immunology and Allergy
    • Immunology

    Cite this

    Host intestinal intraepithelial γδ T lymphocytes present during acute graft‐versus‐host disease in mice may contribute to the development of enteropathy. / Sakai, Tetsu; Ohara‐Inagaki, Kyoko; Tsuzuki, Toyonori; Yoshikai, Yasunobu.

    In: European Journal of Immunology, Vol. 25, No. 1, 01.01.1995, p. 87-91.

    Research output: Contribution to journalArticle

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