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In this study, we show that mice lacking the protein tyrosine phosphatase Shp1 specifically in DCs develop splenomegaly associated with more CD11c+ DCs. Splenic DCs from the mutant mice showed upregulation of CD86 and CCR7 expression and of LPS-induced production of proinflammatory cytokines. The mice manifested more splenic Th1 cells, consistent with the increased ability of their DCs to induce production of IFN-\u03b3 by Ag-specific T cells in vitro. The number of splenic CD5+CD19+ B-1a cells and the serum concentrations of Igs M and G2a were also increased in the mutant mice. Moreover, aged mutant mice developed glomerulonephritis and interstitial pneumonitis together with increased serum concentrations of autoantibodies. Shp1 is thus a key regulator of DC functions that protects against autoimmunity.<\/jats:p>","DOI":"10.4049\/jimmunol.1103210","type":"journal-article","created":{"date-parts":[[2012,4,27]],"date-time":"2012-04-27T00:31:11Z","timestamp":1335486671000},"page":"5397-5407","source":"Crossref","is-referenced-by-count":54,"title":["Dendritic Cell-Specific Ablation of the Protein Tyrosine Phosphatase Shp1 Promotes Th1 Cell Differentiation and Induces Autoimmunity"],"prefix":"10.1093","volume":"188","author":[{"given":"Tetsuya","family":"Kaneko","sequence":"first","affiliation":[{"name":"Laboratory of Biosignal Sciences, Institute for Molecular and Cellular Regulation, Gunma University , Maebashi, Gunma 371-8512 ,","place":["Japan"]},{"name":"Department of Orthopedic Surgery, Gunma University Graduate School of Medicine , Maebashi, Gunma 371-8511 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