Home Basic Science • Advances in Immunology 50 by Frank J. Dixon

Advances in Immunology 50 by Frank J. Dixon

By Frank J. Dixon

The fiftieth quantity in a monographic sequence on immunology. one of the issues coated listed here are avian T-cell ontogeny, adoptive move of human lymphoid cells to critically immuno-deficient mice and histamine-releasing components and cytokine-dependent activation of basophils and mast cells.

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Vp SELECTIVE ELEMENTS 27 Taken together, these data are most consistent with the consensus model, stating that the critical contact sites between Vbse or bacterial toxic mitogens and the Vp region of the TCR lie on the lateral face of the TCR Vp domain and are encoded in the adjacent loops involving amino acids 67-77 and amino acid 22. The involvement of the TCR loops equivalent to CDRs 1, 2, and 3 in these responses requires further analysis. Are the changes observed in this region consistent, or do they reflect particular MHC and Vbse combinations.

1991). , 1988; Tomonari and Lovering, 1988). Vp SELECTIVE ELEMENTS 25 Some of the residual cells can respond to antireceptor antibody. This suggests that more subtle aspects of the interaction between the TCR, MHC class 11, and the Vbse may involve p chain VDJ junctions or the a chain of the receptor. Under conditions of limited stimulation, these differences may be critical. 3. Mapping Relevant Sites on the T Cell Receptor Vp Region Having identified the Vp-encoded segment of the TCR as the critical site of action of Vbse, Kappler, Marrack and co-workers sought pairs of closely related Vp that differed in their reactivity to Vbse.

4. A modification o f t h e working model to account for anomalies seen in various studies. (A) Several studies suggest that Mls-like proteins participate in antigen recognition, serving to stabilize or orient the T cell receptor to its MHC class I1 ligand. We have termed such structures coligands. (B) The current working model, as in Fig. 1B. (C) A modified model of stimulation by the staphylococcal enterotoxins (SE) in which the SE binds to MHC class I1 and the coligand, allowing the coligand to interact with the VP domain of the T cell receptor with sufficient strength to stiniulate the T cell.

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