title: Co-stimulatory signals increase the reactivity of gammadelta T cells towards mycobacterial antigens.
abstract: Although it has been shown that gammadelta T lymphocytes are able to react with different cell-associated or soluble antigens, the immune repertoire of these cells appears to be skewed to the recognition of mycobacterial antigens. We have studied the number and reactivity of gammadelta T cells towards several mycobacterial antigens in patients with tuberculosis and leprosy, as well as their healthy contacts and control individuals. We found an increased number of Vdelta2+ cells in healthy contacts (PPD+ and lepromin+) and tuberculoid leprosy patients. The gammadelta T cells from lepromatous leprosy showed a decreased response to all antigens tested, but some of these patients exhibited a significant response to the 30-kD glycoprotein of Mycobacterium tuberculosis. Interestingly, the reactivity of gammadelta T cells against mycobacterial antigens was significantly increased by costimulatory signals generated through CD7, LFA-1, CD50 and CD69 in all groups. However, signalling through CD69 did not enhance the responsiveness of gammadelta lymphocytes from lepromatous patients. On the other hand, the in vitro blockade of IL-10 with a specific antibody enhanced the cell proliferation of gammadelta lymphocytes from lepromatous leprosy patients, whereas exogenous IL-10 had an opposite effect in most individuals studied. These results suggest the potential role of different cell membrane receptors in the regulation of gammadelta T cell proliferation induced by mycobacteria, as well as the possible involvement of IL-10 in this phenomenon.
authors.affiliation: Department of Immunology, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí, S.L.P, México, D.F., México. rgonzale@deimos.tc.uaslp.mx
authors.forename: R
authors.initials: R
authors.lastname: González-Amaro
authors.forename: D P
authors.initials: DP
authors.lastname: Portales-Pérez
authors.forename: L
authors.initials: L
authors.lastname: Baranda
authors.forename: B
authors.initials: B
authors.lastname: Moncada
authors.forename: C
authors.initials: C
authors.lastname: Toro
authors.forename: S
authors.initials: S
authors.lastname: López-Briones
authors.forename: C
authors.initials: C
authors.lastname: Espitia
authors.forename: R
authors.initials: R
authors.lastname: Mancilla
mesh_terms: D000911:Antibodies, Monoclonal; D000942:Antigens, Bacterial / Q000276:immunology*; D015703:Antigens, CD / Q000276:immunology; D019011:Antigens, CD7 / Q000276:immunology; D000943:Antigens, Differentiation; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000276:immunology; D002455:Cell Division; D002469:Cell Separation; D002478:Cells, Cultured; D005434:Flow Cytometry; D006801:Humans; D016753:Interleukin-10 / Q000037:antagonists & inhibitors; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D016169:Lymphocyte Function-Associated Antigen-1 / Q000276:immunology; D009161:Mycobacterium / Q000276:immunology*; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000276:immunology*; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology*; D000099192:CD69 Antigens
chemical_list: D000911:Antibodies, Monoclonal; D000942:Antigens, Bacterial; D015703:Antigens, CD; D019011:Antigens, CD7; D000943:Antigens, Differentiation; D000945:Antigens, Differentiation, T-Lymphocyte; D015815:Cell Adhesion Molecules; D016753:Interleukin-10; D037181:Lectins, C-Type; D016169:Lymphocyte Function-Associated Antigen-1; D016692:Receptors, Antigen, T-Cell, gamma-delta; D000099192:CD69 Antigens; C483616:ICAM3 protein, human