• Media type: E-Article
  • Title: Dendritic cells control CD4+CD25+ Treg cell function in vitro through juxtacrine delivery of IL-2. (50.3)
  • Contributor: Field, Elizabeth; Kulhankova, Katarina; Rouse, Todd; Nasr, Mohamed
  • imprint: The American Association of Immunologists, 2011
  • Published in: The Journal of Immunology
  • Language: English
  • DOI: 10.4049/jimmunol.186.supp.50.3
  • ISSN: 0022-1767; 1550-6606
  • Keywords: Immunology ; Immunology and Allergy
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title> <jats:p>CD4+CD25+ regulatory T cells (Tregs) require IL-2 for their expansion and function. Unable to produce IL-2, Tregs rely on IL-2 from a neighboring cell. We explored whether DCs might serve as an important source of IL-2 for Tregs. Though a minor subset of DCs make IL-2, the IL-2 producing DCs were preferentially found in conjugate formation with Tregs. DCs continued to transcribe IL-2 in the presence of Tregs, but protein secretion was completely diverted to the Treg. Uptake of DC-derived IL-2 by Tregs involved cell:cell contact and CD25. DC IL-2 increased Tregs levels of CD25 and foxp3. Surprisingly, Treg suppressor function in vitro depended on DC IL-2. Tregs in cultures with WT DCs suppressed proliferation of CD4+ Teff more effectively than Tregs in cultures with IL-2 KO DCs. Tregs also suppressed IL-2 secretion by CD4+ Teff if cultured with WT DCs but showed no suppression if cultured with IL-2 KO DCs. In the later cultures, the transient addition of IL-2 at levels ≥ 500 U/ml restored Treg suppressor function, suggesting that DC to Treg delivery of IL-2 was spatially controlled to achieve locally high concentrations of IL-2. The findings demonstrate a clear requirement for DC-derived IL-2 for optimal Treg suppressor function in vitro and reveal a novel model of juxtacrine delivery of IL-2 from DCs to Tregs. The data lead us to speculate that IL-2 producing DCs may play a role in initiating the activation of functional Tregs in vivo through spatial delivery of signal 3.</jats:p>
  • Access State: Open Access