title: Phenotypic and functional analysis of CD4+ NKRP1A+ human T lymphocytes. Direct evidence that the NKRP1A molecule is involved in transendothelial migration.
abstract: In this report, we show that among human CD4+ T lymphocytes 5-20% express the C-type lectin molecule NKRP1A. This lymphocyte subset displays a slightly more limited T cell receptor V beta repertoire than the CD4+ NKRP1A- counterpart. CD4+ NKRP1A+ T lymphocytes are characterized by a high expression of beta 1 and beta 2 integrins, thus representing a T lymphocyte subset that can possibly adhere and migrate through vascular endothelium. Indeed, resting CD4+ NKRP1A+ lymphocytes, differently from the CD4+ NKRP1A- subset, migrated across endothelial cell monolayers in a Transwell chamber system. Pretreatment of CD4+ NKRP1A+ T lymphocytes with an anti-NKRP1A monoclonal antibody (mAb) strongly reduced transendothelial migration, suggesting the involvement of the NKRP1A molecule in the transmigration process. Furthermore, cells of the NKRP1A- Jurkat CD4+ T cell line stably transfected with NKRP1A cDNA migrated more rapidly and efficiently than either untransfected or mock-transfected Jurkat cells. Finally, mAb-mediated cross-linking of NKRP1A molecules in CD4+ T lymphocytes induced the up-regulation of the lymphocyte function-associated antigen 1 Mg(2+)-binding site as well as beta 1 and beta 2 integrin chains. Altogether, these findings suggest that the NKRP1A molecule is involved in transendothelial migration of resting CD4+ T lymphocytes.
authors.affiliation: Istituto Nazionale per la Ricerca sul Cancro e Centro di Biotecnologie Avanzate, Genova, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Poggi
authors.forename: P
authors.initials: P
authors.lastname: Costa
authors.forename: M R
authors.initials: MR
authors.lastname: Zocchi
authors.forename: L
authors.initials: L
authors.lastname: Moretta
mesh_terms: D000954:Antigens, Surface / Q000502:physiology*; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology* / Q000276:immunology / Q000502:physiology; D002465:Cell Movement; D004727:Endothelium / Q000166:cytology; D006801:Humans; D016023:Integrins / Q000378:metabolism*; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D016131:Lymphocyte Subsets / Q000166:cytology* / Q000276:immunology / Q000502:physiology; D055651:NK Cell Lectin-Like Receptor Subfamily B; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000378:metabolism; D011971:Receptors, Immunologic / Q000502:physiology*; D014407:Tumor Cells, Cultured; D015854:Up-Regulation
chemical_list: D000954:Antigens, Surface; D016023:Integrins; C527203:KLRB1 protein, human; D037181:Lectins, C-Type; D016169:Lymphocyte Function-Associated Antigen-1; D055651:NK Cell Lectin-Like Receptor Subfamily B; D016693:Receptors, Antigen, T-Cell, alpha-beta; D011971:Receptors, Immunologic