title: Resistance of extrathymic T cells to stress and the role of endogenous glucocorticoids in stress associated immunosuppression.
abstract: When mice were exposed to restraint stress for 12 or 24 h, severe lymphopenia was induced in all immune system organs, including the liver and the thymus. However, in adrenalectomized mice, this response was completely absent. Phenotypic characterization revealed that interleukin (IL)-2Rbeta+CD3int cells (i.e. extrathymic T cells) with CD4+ phenotype and the NK1.1+ subset of CD3int cells (i.e. NKT cells) in the liver as well as the mature conventional T cells in the thymus were resistant to such stress. In adrenalectomized mice, there was no significant change in the distribution of lymphocyte subsets in all tested organs before stress. Interestingly, the number of lymphocytes in the liver and spleen and the proportion of NKT cells in the liver rather increased after stress in these adrenalectomized mice. Therefore, endogenous steroid hormones were indicated to be important in the induction of immunosuppressive states after stress. Among stress associated cytokines, the secretion of tumour necrosis factor (TNF)-alpha was completely suppressed while that of IL-6 was partially suppressed in adrenalectomized mice. These results suggest that endogenous steroid hormones are important for the induction of the stress associated immunosuppression and that NKT cells are resistant to stress, namely, resistant to exposure to endogenous steroid hormones.
authors.affiliation: Department of Immunology, and; First Department of Surgery, Niigata University School of Medicine, Niigata 951-8510, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Shimizu
authors.forename: T
authors.initials: T
authors.lastname: Kawamura
authors.forename: C
authors.initials: C
authors.lastname: Miyaji
authors.forename: H
authors.initials: H
authors.lastname: Oya
authors.forename: M
authors.initials: M
authors.lastname: Bannai
authors.forename: S
authors.initials: S
authors.lastname: Yamamoto
authors.forename: A
authors.initials: A
authors.lastname: Weerasinghe
authors.forename: R C
authors.initials: RC
authors.lastname: Halder
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Hatakeyama
authors.forename: T
authors.initials: T
authors.lastname: Abo
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D017252:CD3 Complex / Q000096:biosynthesis; D002395:Catecholamines / Q000097:blood; D003345:Corticosterone / Q000097:blood; D003593:Cytoplasm / Q000276:immunology / Q000378:metabolism; D005938:Glucocorticoids / Q000097:blood / Q000502:physiology*; D007113:Immunity, Innate; D016130:Immunophenotyping; D007165:Immunosuppression Therapy; D015850:Interleukin-6 / Q000097:blood; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism; D008099:Liver / Q000166:cytology / Q000276:immunology*; D016131:Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D012149:Restraint, Physical; D013154:Spleen / Q000166:cytology / Q000276:immunology*; D013312:Stress, Physiological / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D017252:CD3 Complex; D002395:Catecholamines; D005938:Glucocorticoids; D015850:Interleukin-6; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; D003345:Corticosterone