Search for: [Abstract = "ffector and regulating mechanisms of CHS mediated by Th1 CD4\+ lymphocytes are well known, which may contribute to the development of new methods of contact skin inflammation treatment.In this dissertation, it was investigated whether the EC immunization with a DNP\-coupled protein antigen can suppress Tc1 CD8\+\-mediated contact hypersensitivity in BALB\/c mice. We have found that EC immunization with DNP\-conjugated bovine serum albumin \(DNP\-BSA\) prior to sensitization with 0.5% dinitrofluorobenzene \(DNFB\) did indeed suppress Tc1 CD8\+\-mediated CHS in vivo when compared with positive control. The observed reduction of ear swelling was correlating with the depression of vascular permeability, ear weight, IFN\-γ concentration and MPO activity in ear homogenates. These results were confirmed by an in vitro model, where EC deposition of a protein antigen suppressed proliferation of Tef cells. It was also shown that DNP\-BSA application prior to sensitization with DNFB significantly inhibited production of pro\-inflammatory IFN\-γ, IL\-12 and TNF\-α.In a further experiment it was determined that the optimal dose of EC\-applied DNP\-BSA which could suppress CHS ranges between 100 and 3 µg of antigen \/ mouse and that the state of unresponsiveness declined with time and lasted for around three weeks. \; Experiments in a model of an active immunization, “transfer in” and adoptive cell transfer of CHS"]

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