Abstract:
:Plasmacytoid dendritic cells (pDCs) are primary producers of type I interferon (IFN) in response to viruses. The IFN-producing capacity of pDCs is regulated by specific inhibitory receptors, yet none of the known receptors are conserved in evolution. We report that within the human immune system, receptor protein tyrosine phosphatase sigma (PTPRS) is expressed specifically on pDCs. Surface PTPRS was rapidly downregulated after pDC activation, and only PTPRS(-) pDCs produced IFN-α. Antibody-mediated PTPRS crosslinking inhibited pDC activation, whereas PTPRS knockdown enhanced IFN response in a pDC cell line. Similarly, murine Ptprs and the homologous receptor phosphatase Ptprf were specifically co-expressed in murine pDCs. Haplodeficiency or DC-specific deletion of Ptprs on Ptprf-deficient background were associated with enhanced IFN response of pDCs, leukocyte infiltration in the intestine and mild colitis. Thus, PTPRS represents an evolutionarily conserved pDC-specific inhibitory receptor, and is required to prevent spontaneous IFN production and immune-mediated intestinal inflammation.
journal_name
Immunityjournal_title
Immunityauthors
Bunin A,Sisirak V,Ghosh HS,Grajkowska LT,Hou ZE,Miron M,Yang C,Ceribelli M,Uetani N,Chaperot L,Plumas J,Hendriks W,Tremblay ML,Häcker H,Staudt LM,Green PH,Bhagat G,Reizis Bdoi
10.1016/j.immuni.2015.07.009subject
Has Abstractpub_date
2015-08-18 00:00:00pages
277-88issue
2eissn
1074-7613issn
1097-4180pii
S1074-7613(15)00276-9journal_volume
43pub_type
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