PMID- 27815439
OWN - NLM
STAT- MEDLINE
DCOM- 20170811
LR  - 20180124
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 197
IP  - 10
DP  - 2016 Nov 15
TI  - Are Regulatory T Cells Defective in Type 1 Diabetes and Can We Fix Them?
PG  - 3762-3770
AB  - Regulatory T cells (Tregs) are critical regulators of peripheral immune
      tolerance. Treg insufficiency can lead to autoimmune disorders, including type 1 
      diabetes (T1D). Increasing evidence in mouse models of T1D, as well as other
      autoimmune disorders, suggests that there are defects in Treg-mediated
      suppression. Indeed, whereas Treg frequency in the peripheral blood of T1D
      patients is unaltered, their suppressive abilities are diminished compared with
      Tregs in healthy controls. Although expression of the transcription factor Foxp3 
      is a prerequisite for Treg development and function, there are many additional
      factors that can alter their stability, survival, and function. Much has been
      learned in other model systems, such as tumors, about the mechanism and pathways 
      that control Treg stability and function. This review poses the question of
      whether we can use these findings to develop new therapeutic approaches that
      might boost Treg stability, survival, and/or function in T1D and possibly other
      autoimmune disorders.
CI  - Copyright (c) 2016 by The American Association of Immunologists, Inc.
FAU - Visperas, Anabelle
AU  - Visperas A
AD  - Department of Immunology, University of Pittsburgh School of Medicine,
      Pittsburgh, PA 15213; and.
FAU - Vignali, Dario A A
AU  - Vignali DA
AD  - Department of Immunology, University of Pittsburgh School of Medicine,
      Pittsburgh, PA 15213; and dvignali@pitt.edu.
AD  - Tumor Microenvironment Center, University of Pittsburgh Cancer Institute,
      Pittsburgh, PA 15232.
LA  - eng
GR  - P01 AI108545/AI/NIAID NIH HHS/United States
GR  - R01 DK089125/DK/NIDDK NIH HHS/United States
GR  - T32 AI089443/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Review
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Forkhead Transcription Factors)
SB  - AIM
SB  - IM
MH  - Animals
MH  - Autoimmune Diseases/immunology
MH  - Diabetes Mellitus, Type 1/*immunology/physiopathology/therapy
MH  - Disease Models, Animal
MH  - Forkhead Transcription Factors/metabolism
MH  - Gene Expression Regulation
MH  - Humans
MH  - *Immune Tolerance
MH  - Mice
MH  - T-Lymphocytes, Regulatory/*immunology/*physiology
PMC - PMC5119643
MID - NIHMS810516
EDAT- 2016/11/07 06:00
MHDA- 2017/08/12 06:00
CRDT- 2016/11/06 06:00
PHST- 2016/06/27 00:00 [received]
PHST- 2016/07/27 00:00 [accepted]
PHST- 2016/11/06 06:00 [entrez]
PHST- 2016/11/07 06:00 [pubmed]
PHST- 2017/08/12 06:00 [medline]
AID - 197/10/3762 [pii]
AID - 10.4049/jimmunol.1601118 [doi]
PST - ppublish
SO  - J Immunol. 2016 Nov 15;197(10):3762-3770. doi: 10.4049/jimmunol.1601118.