Jameson fink pdf#

Preferential positive selection of V alpha 2+ CD8+ T cells in mouse strains expressing both H-2k and T cell receptor V alpha a haplotypes: determination with a V alpha 2-specific monoclonal antibody. Pircher H, Rebaï N, Groettrup M, Grégoire C, Speiser DE, Happ MP, Palmer E, Zinkernagel RM, Hengartner H, Malissen B.Transgene detection in unpurified mouse tail DNA by polymerase chain reaction. Resting and anergic B cells are defective in CD28-dependent costimulation of naive CD4+ T cells. Ho WY, Cooke MP, Goodnow CC, Davis MM.Complete dissection of the Hb(64-76) determinant using T helper 1, T helper 2 clones, and T cell hybridomas. Evavold BD, Williams SG, Hsu BL, Buus S, Allen PM.Th2 cell clonal anergy as a consequence of partial activation. Sloan-Lancaster J, Evavold BD, Allen PM.Induction of T-cell anergy by altered T-cell-receptor ligand on live antigen-presenting cells. Antagonism of superantigen-stimulated helper T-cell clones and hybridomas by altered peptide ligand. Evavold BD, Sloan-Lancaster J, Allen PM.Separation of IL-4 production from Th cell proliferation by an altered T cell receptor ligand. Signals and signs for lymphocyte responses. Tickling the TCR: selective T-cell functions stimulated by altered peptide ligands.

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Jameson fink pdf#

The Full Text of this article is available as a PDF (738K). These results highlight how specificity guides developing T cells through a network of ligands and indicate that the endogenous peptide pool has a profound effect on T cell development and repertoire. Endogenous presentation of the antagonist ligand in the thymus selectively eliminated the high-avidity cells, while sparing low-avidity cells in the Ser69-reactive T cell repertoire. Thus, in this unique experimental system, Ser69 became an agonist, and Hbd (64-76) was an antagonist. A majority reacted only to Ser69, and not to Hbd(64-76) in fact, Hbd(64-76) was a specific TCR antagonist for these Ser69-only-reactive T cells. A smaller population of the Ser69-reactive T cells responded both to Ser69 and Hbd (64-76).

Two Ser69-reactive T cell populations were identified. This led to a serendipitous primary reactivity to Ser69 peptide, an altered peptide ligand of the Hbd (64-76) epitope of the parent clone. In these mice, the transgenic beta chains paired with endogenous alpha chains. We examined the impact of an endogenous peptide on in vivo T cell development, using a TCR transgenic mouse model based on a hemoglobin-specific T cell clone. T cells potentially encounter numerous endogenous peptides during selection in the thymus and in the periphery.