Dissection of the poly(glualatyr) (GAT)-specific T-cell repertoire in H-21 mice - I. GAT plus self-I-A-reactive T-cell clones can recognize alloactivating and/or restriction determinants on nonself-Ia molecules
Immunogenetics, ISSN: 1432-1211, Vol: 18, Issue: 5, Page: 475-488
1983
- 22Citations
- 3Captures
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Metrics Details
- Citations22
- Citation Indexes22
- CrossRef22
- 21
- Captures3
- Readers3
Article Description
We examined the antigen recognition of the class II major histocompatibility complex (MHC) of 45 poly(glualatyr) (GAT)-reactive T-cell clones isolated by limiting dilution cloning of a pool of in vivo-primed and in vitro-restimulated A.TL lymph-node T cells. Each clone expressed the Thy-1.2, Lyt-1, Lyt-2, LFA-1, Ia, and H-2D cell-surface phenotype and exhibited strict specificity for GAT on syngeneic antigen-presenting cells (APCs). The monitoring of the proliferative responses of these clones in the presence or absence of GAT, using APCs from strains with 11 independent H-2 haplotypes, revealed several distinct specificity patterns: (i) most (31 of 45, 73%) T-cell clones recognized GAT in a self-I-A-restricted manner; (ii) other alloreactive clones (5 of 45, 11%) were stimulated to proliferate, irrespective of the presence of GAT, in response to allodeterminants expressed on H-2, H-2, H-2 or H-2 spleen cells; (iii) a third T-cell clone subset (4 of 45, 9%) was activated by GAT in the context of not only self-I-A but also nonself restriction Ia determinants; and (iv) three clones (7%) exhibited a triple specificity, i. e., they recognized GAT in the context of self and nonself Ia determinants and were alloreactive. One of the latter clones responded to GAT in an apparently non-MHC-restricted manner and recognized an I-A allodeterminant. These data provide direct evidence that the antigen-specific and alloreactive T-cell repertoires overlap and that the self-MHC restriction of GAT-specific T-cell responses is not absolute in A.TL mice. © 1983 Springer-Verlag.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0020973402&origin=inward; http://dx.doi.org/10.1007/bf00364389; http://www.ncbi.nlm.nih.gov/pubmed/6196284; http://link.springer.com/10.1007/BF00364389; http://www.springerlink.com/index/pdf/10.1007/BF00364389; http://www.springerlink.com/index/10.1007/BF00364389; https://dx.doi.org/10.1007/bf00364389; https://link.springer.com/article/10.1007/BF00364389
Springer Nature
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