title: [Tc1-mediated contact sensitivity reaction, its mechanism and regulation].
abstract: The contact hypersensitivity reaction (CHS) to haptens is a classic example of cell-mediated immune response. In the effector phase, two stages can be distinguished: an early component, that appears only 2 hours after subsequent contact with the hapten, and the late component that develops approximately 24 hours later which is mediated by TCRαβ+ cells. The effector lymphocytes may be CD4+ T helper 1 (Th1) cells or CD8+ T cytotoxic 1 (Tc1) cells, which depends on the employed hapten and/or mice strain. NKT lymphocytes play the crucial role in the CHS initiation, by supporting B1 cells in the antigen-specific IgM antibodies production. The development of an early component is essential for the recruitment of T effector (Teff) cells to the side of hapten deposition and for the complete expansion of inflammatory reaction. The CHS reaction is under T regulatory (Treg) cells control, both in the induction phase as well as in the effector phase. A new view of a negative regulation of the Tc1 mediated CHS response is based on the suppression induced by epicutaneous (EC) application of protein antigen. The DNP-BSA skin application, on a gauze patch, leads to a state of immunosuppression. This maneuver results in rising the population of Treg cells with TCRαβ+CD4+CD25+Foxp3+ phenotype. The mechanism of suppression requires direct contact between Treg cells and Teff cells and the participation of CTLA-4 molecule is also necessary. The described method of evoking immune tolerance via EC immunization may contribute to elaborate a new method of allergic contact dermatitis therapy. This is because of its effectiveness, ease of induction and non-invasive protein antigen application.
authors: Katedra Biologii Medycznej, Instytut Pielęgniarstwa i Położnictwa UJ CM.
authors: Magdalena
authors: M
authors: Zemelka-Wiącek
authors: Katedra Biologii Medycznej, Instytut Pielęgniarstwa i Położnictwa UJ CM.
authors: Marian
authors: M
authors: Szczepanik
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D017449:Dermatitis, Allergic Contact / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D004140:Dinitrophenols / Q000276:immunology / Q000627:therapeutic use; D006241:Haptens / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D007075:Immunoglobulin M / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D051379:Mice; D012710:Serum Albumin, Bovine / Q000276:immunology / Q000627:therapeutic use; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology* / Q000473:pathology
chemical_list: D000941:Antigens; D004140:Dinitrophenols; D006241:Haptens; D007075:Immunoglobulin M; C034638:dinitrophenyl-bovine serum albumin; D012710:Serum Albumin, Bovine