{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T07:37:55Z","timestamp":1768635475909,"version":"3.49.0"},"reference-count":52,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2010,10,1]],"date-time":"2010-10-01T00:00:00Z","timestamp":1285891200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Galectin-1 (Gal-1), a \u03b2-galactoside\u2013binding lectin, plays a profound role in modulating adaptive immune responses by altering the phenotype and fate of T cells. Experimental data showing recombinant Gal-1 (rGal-1) efficacy on T cell viability and cytokine production, nevertheless, is controversial due to the necessity of using stabilizing chemicals to help retain Gal-1 structure and function. To address this drawback, we developed a mouse Gal-1 human Ig chimera (Gal-1hFc) that did not need chemical stabilization for Gal-1 ligand recognition, apoptosis induction, and cytokine modulation in a variety of leukocyte models. At high concentrations, Gal-1hFc induced apoptosis in Gal-1 ligand+ Th1 and Th17 cells, leukemic cells, and granulocytes from synovial fluids of patients with rheumatoid arthritis. Importantly, at low, more physiologic concentrations, Gal-1hFc retained its homodimeric form without losing functionality. Not only did Gal-1hFc\u2013binding trigger IL-10 and Th2 cytokine expression in activated T cells, but members of the CD28 family and several other immunomodulatory molecules were upregulated. In a mouse model of contact hypersensitivity, we found that a non-Fc receptor-binding isoform of Gal-1hFc, Gal-1hFc2, alleviated T cell-dependent inflammation by increasing IL-4+, IL-10+, TGF-\u03b2+, and CD25high\/FoxP3+ T cells, and by decreasing IFN-\u03b3+ and IL-17+ T cells. Moreover, in human skin-resident T cell cultures, Gal-1hFc diminished IL-17+ T cells and increased IL-4+ and IL-10+ T cells. Gal-1hFc will not only be a useful new tool for investigating the role of Gal-1 ligands in leukocyte death and cytokine stimulation, but for studying how Gal-1\u2013Gal-1 ligand binding shapes the intensity of immune responses.<\/jats:p>","DOI":"10.4049\/jimmunol.1000715","type":"journal-article","created":{"date-parts":[[2010,9,16]],"date-time":"2010-09-16T02:27:36Z","timestamp":1284604056000},"page":"4659-4672","source":"Crossref","is-referenced-by-count":54,"title":["Development of a Nascent Galectin-1 Chimeric Molecule for Studying the Role of Leukocyte Galectin-1 Ligands and Immune Disease Modulation"],"prefix":"10.1093","volume":"185","author":[{"given":"Filiberto","family":"Cedeno-Laurent","sequence":"first","affiliation":[{"name":"Department of Dermatology , Boston, MA 02115"},{"name":"Harvard Medical School , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven R","family":"Barthel","sequence":"additional","affiliation":[{"name":"Department of Dermatology , Boston, MA 02115"},{"name":"Harvard Medical School , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew J","family":"Opperman","sequence":"additional","affiliation":[{"name":"Department of Dermatology , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David M","family":"Lee","sequence":"additional","affiliation":[{"name":"Harvard Medical School , Boston, MA 02115"},{"name":"Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women\u2019s Hospital , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rachael A","family":"Clark","sequence":"additional","affiliation":[{"name":"Department of Dermatology , Boston, MA 02115"},{"name":"Harvard Medical School , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charles J","family":"Dimitroff","sequence":"additional","affiliation":[{"name":"Department of Dermatology , Boston, MA 02115"},{"name":"Harvard Medical School , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2010,10,15]]},"reference":[{"key":"2025032412024240900_r1","doi-asserted-by":"crossref","first-page":"981","DOI":"10.1038\/ni.1772","article-title":"Tolerogenic signals delivered by dendritic cells to T cells through a galectin-1-driven immunoregulatory circuit involving interleukin 27 and interleukin 10","volume":"10","author":"Ilarregui","year":"2009","journal-title":"Nat. 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