{'fraction_non_alphanumeric': 0.0282311424790472, 'fraction_numerical': 0.019850022055580063, 'mean_word_length': 4.349056603773585, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Preferential V beta usage by cytotoxic T cells cross-reactive between two epitopes of HIV-1 gp160 and degenerate in class I MHC restriction.

The T cell response to HIV-1 gp160 is among the most thoroughly studied immune responses to HIV-1 products. In our previous work, the MHC class I molecule Dd as well as H-2u, p, and q, were found to present P18 and HP53, two determinants of HIV-1 gp160, to CD8+ CTL in mice. We have studied the TCR V beta chain expression in CTL lines, either cross-reactive for these two peptides or specific for P18 alone, in these four different MHC haplotypes. The usage of V beta in T cells showing cross-reaction between these two peptides was remarkably conserved (primarily V beta 8 family, with some use of V beta 14) despite the extensive TCR V beta diversity of the non-cross-reactive CTL, which did not use V beta 8 or 14. This correlation of V beta usage with fine specificity was consistent in H-2d, u, and p (p < 0.01), but not in H-2q. The correlation of V beta use with peptide fine specificity independent of MHC restriction was unexpected. The strong predominance of V beta 8 family TCR was all the more surprising in view of the finding that mice bearing a genomic deletion of V beta 8 can still produce T cells with the cross-reactive phenotype, implying that other V beta chains can produce this specificity. We therefore asked whether the complexes of P18 with H-2d, p, and u are recognized as identical, and observed the surprising result that H-2d, p, and u cells mutually cross-present the peptides P18 and HP53 to allogeneic CTL lines and individual clones of each of the other haplotypes, whereas none of these cross-present to H-2q CTL, nor do H-2q targets present to CTL of the other haplotypes. This degeneracy of MHC restriction is novel for class I molecules. Moreover, the observed restriction in V beta usage occurs only in the unique set of CTL that exhibit both peptide-cross-reactive fine specificity and MHC allogeneic cross-presentation. The observation that a strain of mice in which the V beta 8 family is genomically deleted can still make CTL of this phenotype using another V beta demonstrates the plasticity of the class I MHC-restricted repertoire when the dominating receptor is not available.