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Endogenous galectin‐1 enforces class I‐restricted TCR functional fate decisions in thymocytes
Author(s) -
Liu Scot Daren,
Whiting Chan C,
Tomassian Tamar,
Pang Mabel,
Bissel Stephanie J,
Baum Linda G,
Mossine Valeri V,
Poirier Francoise,
Miceli M Carrie
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.661.5
Subject(s) - t cell receptor , agonist , thymocyte , galectin , negative selection , cd8 , context (archaeology) , biology , double negative , microbiology and biotechnology , immunology , t cell , receptor , antigen , genetics , immune system , gene , paleontology , genome
During thymocyte development, the TCR can discriminate MHC/peptide ligands over a narrow range of affinities and translate subtle differences into functional fate decisions. How small differences in TCR input are translated into absolute differences in functional output is unclear. We examined the effects of galectin‐1 ablation in the context of class‐I‐restricted thymocyte development. Galectin‐1 expression opposed partial‐agonist‐driven positive selection, but promoted agonist‐driven negative selection of conventional CD8 + T cells. Further, galectin‐1 promoted TCR agonist‐driven CD8αα IEL development. Mechanistically, galectin‐1 opposed ERK activity in thymocytes undergoing positive selection and promoted the ERK negative‐selection‐signaling signature in thymocytes undergoing negative selection. We propose that galectin‐1 aids in discriminating TCR fate decisions by enforcing agonist and opposing partial‐agonist TCR signals, widening the distinction between TCR‐directed functional fate cues. This work was supported by grant NIH RO1A1056155 to M. C. Miceli. S. D. Liu was supported by the Microbial Pathogenesis Training Grant T32 AI07323‐15, Clinical and Fundamental Immunology Training Grant AI07126‐30, and Warsaw Fellowship.