Identification of cellular sources of IL-2 needed for regulatory T cell development and homeostasis Academic Article uri icon

Overview

MeSH Major

  • Antigens, CD274
  • Arenaviridae Infections
  • CD8-Positive T-Lymphocytes
  • Interleukin-2
  • Lymphocytic choriomeningitis virus

abstract

  • Copyright © 2018 by The American Association of Immunologists, Inc. The cytokine IL-2 is critical for promoting the development, homeostasis, and function of regulatory T (Treg) cells. The cellular sources of IL-2 that promote these processes remain unclear. T cells, B cells, and dendritic cells (DCs) are known to make IL-2 in peripheral tissues. We found that T cells and DCs in the thymus also make IL-2. To identify cellular sources of IL-2 in Treg cell development and homeostasis, we used Il2FL/FLmice to selectively delete Il2 in T cells, B cells, and DCs. Because IL-15 can partially substitute for IL-2 in Treg cell development, we carried out the majority of these studies on an Il15-/-background. Deletion of Il2 in B cells, DCs, or both these subsets had no effect on Treg cell development, either in wild-type (WT) or Il15-/-mice. Deletion of Il2 in T cells had minimal effects in WT mice but virtually eliminated developing Treg cells in Il15-/-mice. In the spleen and most peripheral lymphoid organs, deletion of Il2 in B cells, DCs, or both subsets had no effect on Treg cell homeostasis. In contrast, deletion of Il2 in T cells led to a significant decrease in Treg cells in either WTor Il15-/-mice. The one exception was the mesenteric lymph nodes where significantly fewer Treg cells were observed when Il2 was deleted in both T cells and DCs. Thus, T cells are the sole source of IL-2 needed for Treg cell development, but DCs can contribute to Treg cell homeostasis in select organs.

publication date

  • June 15, 2018

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC5988981

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.1800097

PubMed ID

  • 29728511

Additional Document Info

start page

  • 3926

end page

  • 3933

volume

  • 200

number

  • 12