title: Early appearance of T cell receptor alpha beta + CD4- CD8- T cells with a skewed variable region repertoire after infection with Listeria monocytogenes.
abstract: We found that the number of T cell receptor (TCR) alpha beta + CD4- CD8- T cells increased in the peritoneal cavity on day 5 after an intraperitoneal infection with Listeria monocytogenes strain EGD together with TCR gamma delta + CD4- CD8- T cells. Thereafter, the TCR alpha beta + CD4- CD8- T cells decreased to a normal level by day 14. The TCR alpha beta + CD4- CD8- T cells showed an activated T cell phenotype (L-selectin CD44 +) and expressed CD45/B220 and interleukin-2 receptor beta, but did not express heat stable antigen, which is expressed by the immature CD4- CD8- thymocytes. Furthermore, 20-30% of the TCR alpha beta + CD4- CD8- T cells expressed the NK1.1 natural killer cell marker. Analysis of the TCR V region repertoire of the TCR alpha beta + CD4- CD8- T cells induced by L. monocytogenes infection showed that more than 80% of the TCR alpha beta + CD4- CD8- T cells expressed TCR V beta 8 detected by anti-TCR V beta 8.1 and 8.2 mAb, and a reverse transcription-polymerase chain reaction analysis of V alpha 14 relative to V alpha 11 expression revealed that the TCR alpha beta + CD4- CD8- T cells expressed a higher level of V alpha 14, which was reported to be preferentially expressed by TCR alpha beta + CD4- CD8- thymocytes rather than conventional CD4+ T cells. The TCR alpha beta + CD4- CD8-T cells showed a proliferative response to anti-TCR alpha beta mAb stimulation. In contrast, they showed no response to stimulation with either Listeria antigen or 65-kDa heat shock protein of Mycobacterium bovis, which do stimulate the Listeria-specific TCR alpha beta + CD4- CD8- T cells and the Listeria-induced TCR gamma delta + T cells, respectively. These results suggest that the TCR alpha beta + CD4- CD8- T cells may recognize a restricted set of self antigens induced by L. monocytogenes infection, and that they contribute to host protection at an early stage of infection.
authors.affiliation: Department of Immunology, Kyushu University, Fukuoka, Japan.
authors.forename: G
authors.initials: G
authors.lastname: Matsuzaki
authors.forename: X Y
authors.initials: XY
authors.lastname: Li
authors.forename: T
authors.initials: T
authors.lastname: Kadena
authors.forename: F
authors.initials: F
authors.lastname: Song
authors.forename: K
authors.initials: K
authors.lastname: Hiromatsu
authors.forename: H
authors.initials: H
authors.lastname: Yoshida
authors.forename: K
authors.initials: K
authors.lastname: Nomoto
mesh_terms: D000818:Animals; D001202:Ascitic Fluid / Q000276:immunology; D017252:CD3 Complex / Q000032:analysis; D005260:Female; D005434:Flow Cytometry; D016130:Immunophenotyping; D008089:Listeria monocytogenes / Q000276:immunology; D008088:Listeriosis / Q000276:immunology*; D008213:Lymphocyte Activation; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000378:metabolism*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013997:Time Factors
chemical_list: D017252:CD3 Complex; D016693:Receptors, Antigen, T-Cell, alpha-beta