title: Increased cell surface expression of a newly identified heterodimer on activated blastic T cells.
abstract: A hybridoma (F6C7) was established by fusing NS1 cells with spleen cells of MRL/Mp-+/+ (MRL/+) mice suffering from lpr-GVHD. This F6C7 mAb (IgG2b, kappa) stains a broad spectrum of blood cells at varying intensities in mice and rats. In normal (BALB/c) mice, granulocytes and B cells are highly positive for F6C7-reactive Ag (F6C7-Ag). Thymocytes and peripheral (CD4+ and CD8+) T cells show negative to low intensities. These staining profiles are similar in C57BL/6, AKR/J, C3H/HeJ, and MRL/+ mice. When spleen cells were activated in vitro, a blastic cell population of autoactivated CD4+ and CD8+ T cells showed increased F6C7-Ag expression. Alloactivated CD4+ blastic T cells also showed increased expression of F6C7-Ag, whereas alloactivated CD8+ blastic T cells as well as Con A-activated CD4+ and CD8+ blastic T cells remained at the level of small (nonblastic) cells. These findings suggest that the surface expression of F6C7-Ag is up-regulated in some activation processes of T cells, particularly in autoactivation. Young (2-month-old) MRL/Mp-lpr/lpr (MRL/lpr) mice show staining profiles of F6C7-Ag similar to those of normal mice, except that many more blastic (CD4+ and CD8+) T cells show high F6C7-Ag expression than those of normal mice. A small but significant number of CD4+F6C7-Ag(high) and a much higher number of CD8+F6C7-Ag(high) blastic T cells were observed in the spleen cells of MRL/+ mice suffering from lpr-GVHD. These blastic T cells may exert autoreactivity and participate in the initiation of autoimmune diseases, lymphadenopathy, and lpr-GVHD. Immunoprecipitation and SDS-PAGE revealed that F6C7-Ag is a heterodimer comprised of approximately 78- and 70-kDa molecules without disulfide bonds.
authors.affiliation: First Department of Pathology, Kansai Medical University, Osaka, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Nagata
authors.forename: S
authors.initials: S
authors.lastname: Taketani
authors.forename: T
authors.initials: T
authors.lastname: Nakagawa
authors.forename: N
authors.initials: N
authors.lastname: Hosaka
authors.forename: H
authors.initials: H
authors.lastname: Hisha
authors.forename: R
authors.initials: R
authors.lastname: Tokunaga
authors.forename: S
authors.initials: S
authors.lastname: Ikehara
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D000954:Antigens, Surface / Q000737:chemistry / Q000378:metabolism*; D001324:Autoantigens / Q000737:chemistry / Q000378:metabolism*; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology; D005260:Female; D006086:Graft vs Host Disease / Q000235:genetics / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D011828:Radiation Chimera / Q000276:immunology; D051381:Rats; D017208:Rats, Wistar; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D001324:Autoantigens