title: Expansion of extrathymic T cells as well as granulocytes in the liver and other organs of granulocyte-colony stimulating factor transgenic mice: why they lost the ability of hybrid resistance.
abstract: When we attempted to characterize the immunological state in G-CSF transgenic mice, a large number of not only granulocytes but also lymphoid cells expanded in various immune organs. Such lymphoid cells were present at unusual sites of these organs, e.g., the parenchymal space in the liver. We then determined the phenotype of these lymphoid cells by immunofluorescence tests. It was demonstrated that CD3intIL-2Rbeta+ cells (i.e., extrathymic T cells), including the NK1.1+ subset of CD3int cells (i.e., NKT cells), increased in the liver and all other tested organs. These T cells as well as NK cells mediated NK and NK-like cytotoxicity, especially at youth. However, they were not able to mediate such cytotoxicity in the presence of granulocytes. This result might be associated with deficiency in the hybrid resistance previously ascribed to these mice. In other words, G-CSF transgenic mice had a large number of extrathymic T cells (including NKT cells) and NK cells that mediate hybrid resistance, but their function was suppressed by activated granulocytes. Indeed, these granulocytes showed an elevated level of Ca2+ influx upon stimulation. The present results suggest that, in parallel with overactivation of granulocytes, extrathymic T cells and NK cells are concomitantly activated in number but that their function is suppressed in G-CSF transgenic mice.
authors.affiliation: Department of Immunology, Niigata University School of Medicine, Niigata, Japan; and Department of Pathology, Sapporo Medical University, Sapporo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kawamura
authors.forename: T
authors.initials: T
authors.lastname: Kawamura
authors.forename: Y
authors.initials: Y
authors.lastname: Kokai
authors.forename: M
authors.initials: M
authors.lastname: Mori
authors.forename: A
authors.initials: A
authors.lastname: Matsuura
authors.forename: H
authors.initials: H
authors.lastname: Oya
authors.forename: S
authors.initials: S
authors.lastname: Honda
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: A
authors.initials: A
authors.lastname: Weerashinghe
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Abo
mesh_terms: D000367:Age Factors; D000818:Animals; D001854:Bone Marrow Cells / Q000276:immunology; D017252:CD3 Complex / Q000302:isolation & purification; D020013:Calcium Signaling; D003345:Corticosterone / Q000097:blood; D003602:Cytotoxicity, Immunologic; D004837:Epinephrine / Q000097:blood; D016179:Granulocyte Colony-Stimulating Factor / Q000096:biosynthesis* / Q000235:genetics; D006098:Granulocytes / Q000166:cytology / Q000276:immunology*; D006801:Humans; D007213:Indomethacin; D007694:Killer Cells, Natural / Q000276:immunology; D008099:Liver / Q000166:cytology / Q000276:immunology*; D016131:Lymphocyte Subsets; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic / Q000276:immunology; D015375:Receptors, Interleukin-2 / Q000302:isolation & purification; D011994:Recombinant Proteins / Q000096:biosynthesis; D012149:Restraint, Physical; D013045:Species Specificity; D013312:Stress, Physiological / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*
chemical_list: D017252:CD3 Complex; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins; D016179:Granulocyte Colony-Stimulating Factor; D003345:Corticosterone; D007213:Indomethacin; D004837:Epinephrine