Implications of determinant spreading for immunotherapy

Knowledge about the temporal pattern of appearance of new T cell specificities directed against determinants within the same or different antigens is crucial in designing appropriate therapeutic strategies. Therapeutic approaches based primarily on controlling T cell responses to the initial disease-inducing determinant may not succecd if spreading of response has already occurred. Tolerance induction with peptides comprising encephalitogenic determinants appearing later in the disease may prevent subsequent progression of EAE. Recently, new strategies based on blocking the B7.1-CD28 interaction have been successful in blocking determinant spreading and thereby preventing relapses during the course of EAE. In the case of diabetes in the NOD mice, in which responses to several antigens appear in a hierarchical fashion, administration of GAD to young NOD mice has been successful in preventing the development of clinical disease. Some evidence in the EAE system points to the need for continued activity of the inflammatory T cells directed against the initiating determinant for perpetuation of the spread. Removal or deactivation of the initiating cell, even after determinant spreading has begun, may weaken or eliminate disease progression. Therefore, measures directed to such initiating cclls may be therapeutic despite their late administration.

See also: Antigen presentation via MHC class II molecules; Autoantigens; Autoimmune diseases; B lymphocyte, antigen processing and presentation; Epitopes; Immunodominance; Immunotherapy of autoimmune diseases; T lymphocytes, autoreactive.

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