Treg-Cell-Derived IL-35-Coated Extracellular Vesicles Promote Infectious Tolerance
Jeremy A. Sullivan(University of Wisconsin–Madison), Yusuke Tomita(University of Wisconsin–Madison), Ewa Jankowska−Gan(University of Wisconsin–Madison), Diego Lema(University of Wisconsin–Madison), Matt Arvedson(University of Wisconsin–Madison), Ashita Nair(University of Wisconsin–Madison), William Bracamonte‐Baran(University of Wisconsin–Madison), Ying Zhou(University of Wisconsin–Madison), Kristy Meyer(William S. Middleton Memorial Veterans Hospital), Weixiong Zhong(University of Wisconsin–Madison), Deepali V. Sawant(University of Pittsburgh), Andrea L. Szymczak-Workman(University of Pittsburgh), Qianxia Zhang(University of Pittsburgh), Creg J. Workman(University of Pittsburgh), Seungpyo Hong(University of Wisconsin–Madison), Dario A.A. Vignali(UPMC Hillman Cancer Center), William J. Burlingham(University of Wisconsin–Madison)
Cited by 158Open Access
Abstract
(iTr35) T cells. Furthermore, IL-35 producers, although rare, secrete Ebi3 and p35 on extracellular vesicles (EVs) targeting a 25- to 100-fold higher number of T and B lymphocytes, causing them to acquire surface IL-35. This surface IL-35 is absent when EV production is inhibited or if Ebi3 is genetically deleted in Treg cells. The unique ability of EVs to coat bystander lymphocytes with IL-35, promoting exhaustion in, and secondary suppression by, non-Treg cells identifies a novel mechanism of infectious tolerance.
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