{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:09:40Z","timestamp":1791223780543,"version":"4.1.0"},"reference-count":62,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T00:00:00Z","timestamp":1406851200000},"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":[[2014,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>T cell exhaustion is thought to be a natural mechanism for limiting immune pathology, although it may be desirable to circumvent this mechanism to help eliminate viral reservoirs or tumors. Although there are no definitive markers, a fingerprint for exhausted T cells has been described that includes the transmembrane proteins PD-1, LAG3, and Tim-3. However, apart from the recruitment of tyrosine phosphatases to PD-1, little is known about the biochemical mechanisms by which these proteins contribute to the development or maintenance of exhaustion. Tim-3 contains no known motifs for the recruitment of inhibitory phosphatases, but it may actually increase signaling downstream of TCR\/CD3, at least under acute conditions. Other studies showed that T cell exhaustion results from chronic stimulation that extends the effector phase of T cell activation, at the expense of T cell memory. We suggest that Tim-3 may contribute to T cell exhaustion by enhancing TCR-signaling pathways.<\/jats:p>","DOI":"10.4049\/jimmunol.1400557","type":"journal-article","created":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T23:16:01Z","timestamp":1406934961000},"page":"1525-1530","source":"Crossref","is-referenced-by-count":164,"title":["Too Much of a Good Thing? Tim-3 and TCR Signaling in T Cell Exhaustion"],"prefix":"10.1093","volume":"193","author":[{"given":"Robert L","family":"Ferris","sequence":"first","affiliation":[{"name":"Department of Immunology, University of Pittsburgh School of Medicine , Pittsburgh, PA 15261"},{"name":"Department of Otolaryngology, University of Pittsburgh School of Medicine , Pittsburgh, PA 15261"},{"name":"Cancer Immunology Program, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine , Pittsburgh, PA 15261"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binfeng","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Pittsburgh School of Medicine , Pittsburgh, PA 15261"},{"name":"Cancer Immunology Program, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine , Pittsburgh, PA 15261"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5198-516X","authenticated-orcid":false,"given":"Lawrence P","family":"Kane","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Pittsburgh School of Medicine , Pittsburgh, PA 15261"},{"name":"Cancer Immunology Program, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine , Pittsburgh, PA 15261"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,8,15]]},"reference":[{"key":"2025030707293436100_r1","doi-asserted-by":"crossref","first-page":"30","DOI":"10.1016\/j.cell.2009.06.036","article-title":"Redefining chronic viral infection","volume":"138","author":"Virgin","year":"2009","journal-title":"Cell"},{"key":"2025030707293436100_r2","doi-asserted-by":"crossref","first-page":"492","DOI":"10.1038\/ni.2035","article-title":"T cell exhaustion","volume":"12","author":"Wherry","year":"2011","journal-title":"Nat. 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