title: Positive regulatory gamma delta T cells in contact sensitivity: augmented responses by in vivo treatment with anti-gamma delta monoclonal antibody, or anti-V gamma 5 or V delta 4.
abstract: Contact sensitivity (CS) responses, induced by skin painting with reactive haptens like picryl chloride or oxazolone, are classical examples of in vivo immunity mediated by alpha beta T cells. Our previous studies showed that gamma delta T cells were required to assist the alpha beta CS-effector T cells in the successful adoptive cell transfer of CS responses. These spleen and lymph node-derived gamma delta+ CS-assisting regulatory cells were CD3+, CD4-CD8+, non-antigen-specific, and non-MHC-restricted, and preferentially expressed V gamma 5 and V delta 4 variable regions. In the current study we show that systemic treatment of mice in vivo with anti-gamma delta mAb, produced a similar positive influence on CS responses in two different systems: i.e. active sensitization, or adoptive cell transfer. In addition to augmented CS responses produced by treatment with pan anti-gamma delta TCR mAb, anti-gamma delta-V region mAb were examined, and augmentation of CS also was produced by anti-V gamma 5 and anti-V delta 4 mAb, the V regions determined previously to be preferentially expressed on gamma delta CS-assisting cells. We speculate that the positive influence of anti-gamma delta mAb was not caused by quantitative changes in gamma delta T cells, because FACS studies demonstrated a lack of in vivo depletion of peripheral blood and lymphoid gamma delta T cells, and also no depletion of epidermal dendritic gamma delta T cells (DETC), in mice treated with anti-gamma delta TCR mAb. Instead, our data favor the hypothesis that CS-assisting gamma delta T cells can be activated in vivo by anti-gamma delta TCR mAb interacting with their gamma delta TCR, at least with the short term protocols we employed, resulting in augmentation of CS responses perhaps by releasing positively-acting factors, such as certain cytokines.
authors.affiliation: Dept. of Immunology, Jagellonian Univ. College of Med., Krakow, Poland.
authors.forename: M
authors.initials: M
authors.lastname: Szczepanik
authors.forename: J
authors.initials: J
authors.lastname: Lewis
authors.forename: G P
authors.initials: GP
authors.lastname: Geba
authors.forename: W
authors.initials: W
authors.lastname: Ptak
authors.forename: P W
authors.initials: PW
authors.lastname: Askenase
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D003877:Dermatitis, Contact / Q000276:immunology*; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D007135:Immunoglobulin Variable Region / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008808:Mice, Inbred CBA; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D007135:Immunoglobulin Variable Region; D016692:Receptors, Antigen, T-Cell, gamma-delta