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Published on: November 4, 2016
Immunological signals which control T cell responses
P M Flood1, O Washington, D P Stevens
1Department of Periodontics, University of North Carolina School of Dentistry, Chapel Hill, USA.
A number of identifiable immunological parameters can influence the elicitation and regulation of antigen-specific inflammatory responses to immunogenic epitopes. Injection of antigen in vivo can lead to the activation of type IV hypersensitivity responses, or to the induction of immunological tolerance to that antigen. We have used the hapten trinitrophenol as a model system for studying the factors which influence the generation and regulation of hypersensitivity responses to immunogenic epitopes in vivo. The generation of hypersensitivity or tolerance to trinitrophenyl depends on a number of immunological factors, including the form of the antigen, the route of immunization, and the presence of immune complexes of antibody and antigen on the surface of the antigen-presenting cell. Immunization with trinitrophenyl resulting in unresponsiveness can be the result of either the inability to prime inflammatory cells in vivo or the induction of suppressor T cells.
A number of identifiable immunological parameters can influence the elicitation and regulation of antigen-specific inflammatory responses to immunogenic epitopes. Injection of antigen in vivo can lead to the activation of type IV hypersensitivity responses, or to the induction of immunological tolerance to that antigen. We have used the hapten trinitrophenol as a model system for studying the factors which influence the generation and regulation of hypersensitivity responses to immunogenic epitopes in vivo. The generation of hypersensitivity or tolerance to trinitrophenyl depends on a number of immunological factors, including the form of the antigen, the route of immunization, and the presence of immune complexes of antibody and antigen on the surface of the antigen-presenting cell. Immunization with trinitrophenyl resulting in unresponsiveness can be the result of either the inability to prime inflammatory cells in vivo or the induction of suppressor T cells.
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