PMID- 27007674
OWN - NLM
STAT- MEDLINE
DCOM- 20171103
LR  - 20230203
IS  - 1935-3456 (Electronic)
IS  - 1933-0219 (Print)
IS  - 1933-0219 (Linking)
VI  - 9
IP  - 6
DP  - 2016 Nov
TI  - Regulatory T cells are essential to promote proper CD4 T-cell priming upon 
      mucosal infection.
PG  - 1395-1406
LID - 10.1038/mi.2016.19 [doi]
AB  - Regulatory T cells (Tregs) limit autoimmunity and immunopathology using a variety 
      of suppressive mechanisms, but their roles during pathogen-directed immune 
      responses remain unclear. Following herpes simplex virus-2 (HSV-2) infection, 
      mice lacking Tregs fail to control viral replication, pointing to a role for 
      Tregs in facilitating productive immune responses. Using adoptive transfer of 
      T-cell receptor transgenic CD4 T cells into Treg-sufficient or Treg-depleted mice 
      prior to HSV-2 infection, we found that Tregs are required for timely 
      accumulation of HSV-2-specific CD4 T cells within the infected tissues. Further, 
      Tregs are critical for appropriate trafficking of dendritic cells (DCs) from the 
      vaginal mucosa to the draining lymph nodes, which results in fully effective CD4 
      T-cell priming, activation, and ultimately migration to the infected tissues. 
      Using CTLA-4 conditional knockout mice, we demonstrate that Tregs impact DC 
      migration through a CTLA-4-mediated mechanism. Together, our data highlight the 
      critical role of Tregs in proper potentiation of adaptive immune responses to 
      microbial infection.
FAU - Soerens, A G
AU  - Soerens AG
AD  - Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, 
      Seattle, Washington, USA.
AD  - Graduate Program in Pathobiology, Department of Global Health, University of 
      Washington, Seattle, Washington, USA.
FAU - Da Costa, A
AU  - Da Costa A
AD  - Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, 
      Seattle, Washington, USA.
AD  - Graduate Program in Pathobiology, Department of Global Health, University of 
      Washington, Seattle, Washington, USA.
FAU - Lund, J M
AU  - Lund JM
AD  - Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, 
      Seattle, Washington, USA.
AD  - Graduate Program in Pathobiology, Department of Global Health, University of 
      Washington, Seattle, Washington, USA.
LA  - eng
GR  - R01 AI087657/AI/NIAID NIH HHS/United States
GR  - T32 AI083203/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20160323
PL  - United States
TA  - Mucosal Immunol
JT  - Mucosal immunology
JID - 101299742
RN  - 0 (CTLA-4 Antigen)
RN  - 0 (Epitopes)
SB  - IM
MH  - Animals
MH  - CD4-Positive T-Lymphocytes/*immunology/*metabolism
MH  - CTLA-4 Antigen/genetics/metabolism
MH  - Cell Communication/immunology
MH  - Cell Movement/immunology
MH  - Cells, Cultured
MH  - Dendritic Cells/immunology/metabolism
MH  - Disease Models, Animal
MH  - Epitopes/immunology
MH  - Female
MH  - Gene Expression
MH  - Herpes Genitalis/immunology/metabolism
MH  - Herpesvirus 2, Human/immunology
MH  - Host-Pathogen Interactions/*immunology
MH  - Humans
MH  - *Immunity, Mucosal
MH  - Immunomodulation
MH  - Mice
MH  - Models, Biological
MH  - Mucous Membrane/*immunology/*metabolism
MH  - T-Cell Antigen Receptor Specificity/immunology
MH  - T-Lymphocytes, Regulatory/*immunology/*metabolism
MH  - Vagina
PMC - PMC5035160
MID - NIHMS760334
COIS- Disclosure. The authors declare no conflicts of interest.
EDAT- 2016/03/24 06:00
MHDA- 2017/11/04 06:00
PMCR- 2016/10/14
CRDT- 2016/03/24 06:00
PHST- 2015/12/16 00:00 [received]
PHST- 2016/02/05 00:00 [accepted]
PHST- 2016/03/24 06:00 [pubmed]
PHST- 2017/11/04 06:00 [medline]
PHST- 2016/03/24 06:00 [entrez]
PHST- 2016/10/14 00:00 [pmc-release]
AID - S1933-0219(22)00783-8 [pii]
AID - 10.1038/mi.2016.19 [doi]
PST - ppublish
SO  - Mucosal Immunol. 2016 Nov;9(6):1395-1406. doi: 10.1038/mi.2016.19. Epub 2016 Mar 
      23.