{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T15:54:42Z","timestamp":1791215682216,"version":"4.1.0"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2010,3,1]],"date-time":"2010-03-01T00:00:00Z","timestamp":1267401600000},"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":[[2010,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Little is known about target organ-infiltrating NK cells in type 1 diabetes and other autoimmune diseases. In this study, we identified NK cells with a unique phenotype in the pancreas of NOD mice. Pancreatic NK cells, localized to the endocrine and exocrine parts, were present before T cells during disease development and did not require T cells for their infiltration. Furthermore, NK cells, or NK cell precursors, from the spleen could traffic to the pancreas, where they displayed the pancreatic phenotype. Pancreatic NK cells from other mouse strains shared phenotypic characteristics with pancreatic NK cells from NOD mice, but displayed less surface killer cell lectin-like receptor G1, a marker for mature NK cells that have undergone proliferation, and also did not proliferate to the same extent. A subset of NOD mouse pancreatic NK cells produced IFN-\u03b3 spontaneously, suggesting ongoing effector responses. However, most NOD mouse pancreatic NK cells were hyporesponsive compared with spleen NK cells, as reflected by diminished cytokine secretion and a lower capacity to degranulate. Interestingly, such hyporesponsiveness was not seen in pancreatic NK cells from the nonautoimmune strain C57BL\/6, suggesting that this feature is not a general property of pancreatic NK cells. Based on our data, we propose that NK cells are sentinel cells in a normal pancreas. We further speculate that during inflammation, pancreatic NK cells initially mediate proinflammatory effector functions, potentially contributing to organ-specific autoimmunity, but later become hyporesponsive because of exhaustion or regulation.<\/jats:p>","DOI":"10.4049\/jimmunol.0804358","type":"journal-article","created":{"date-parts":[[2010,2,3]],"date-time":"2010-02-03T22:10:38Z","timestamp":1265235038000},"page":"2272-2280","source":"Crossref","is-referenced-by-count":83,"title":["Distinct Phenotype and Function of NK Cells in the Pancreas of Nonobese Diabetic Mice"],"prefix":"10.1093","volume":"184","author":[{"given":"Hanna","family":"Brauner","sequence":"first","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Strategic Research Center for Studies of Integrative Recognition in the Immune System"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marjet","family":"Elemans","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Strategic Research Center for Studies of Integrative Recognition in the Immune System"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara","family":"Lemos","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Strategic Research Center for Studies of Integrative Recognition in the Immune System"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Broberger","sequence":"additional","affiliation":[{"name":"Department of Neuroscience"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dan","family":"Holmberg","sequence":"additional","affiliation":[{"name":"Department of Medical Biosciences, Ume\u00e5 University , Ume\u00e5,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malin","family":"Flodstr\u00f6m-Tullberg","sequence":"additional","affiliation":[{"name":"Department of Medicine Huddinge, Center for Infectious Medicine, Karolinska University Hospital Huddinge, Karolinska Institutet , Stockholm"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klas","family":"K\u00e4rre","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Strategic Research Center for Studies of Integrative Recognition in the Immune System"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petter","family":"H\u00f6glund","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Strategic Research Center for Studies of Integrative Recognition in the Immune System"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2010,3,1]]},"reference":[{"key":"2026012806275263100_r1","doi-asserted-by":"crossref","first-page":"613","DOI":"10.1016\/j.it.2005.08.008","article-title":"NK cells: elusive players in autoimmunity.","volume":"26","author":"Johansson","year":"2005","journal-title":"Trends Immunol."},{"key":"2026012806275263100_r2","doi-asserted-by":"crossref","first-page":"757","DOI":"10.1016\/j.immuni.2004.05.008","article-title":"NKG2D blockade prevents autoimmune diabetes in NOD mice.","volume":"20","author":"Ogasawara","year":"2004","journal-title":"Immunity"},{"key":"2026012806275263100_r3","doi-asserted-by":"crossref","first-page":"177","DOI":"10.2337\/db06-0493","article-title":"Altered natural killer cells in type 1 diabetic patients.","volume":"56","author":"Rodacki","year":"2007","journal-title":"Diabetes"},{"key":"2026012806275263100_r4","doi-asserted-by":"crossref","first-page":"5115","DOI":"10.1073\/pnas.0700442104","article-title":"Coxsackie B4 virus infection of \u03b2 cells and natural killer cell insulitis in recent-onset type 1 diabetic patients.","volume":"104","author":"Dotta","year":"2007","journal-title":"Proc. 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