PMID- 29928041
OWN - NLM
STAT- MEDLINE
DCOM- 20181231
LR  - 20190405
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 13
IP  - 6
DP  - 2018
TI  - High level expression of A2ARs is required for the enhancing function, but not
      for the inhibiting function, of gammadelta T cells in the autoimmune responses of
      EAU.
PG  - e0199601
LID - 10.1371/journal.pone.0199601 [doi]
AB  - We previously reported that activated gammadelta T cells greatly enhance
      autoimmune responses, particularly the Th17 response. To determine the mechanisms
      involved, we made a series of comparisons between activated and non-activated
      gammadelta T cells. Our results showed that activated gammadelta T cells
      expressed greatly increased levels of A2A adenosine receptor (A2AR) and decreased
      amounts of CD73, as well as increased amounts of T cell activation markers such
      as CD69, CD44 and CD25. We show that A2AR is a major functional molecule in the
      enhancing activity of gammadelta T cells. A2AR-/- gammadelta T cells (isolated
      from A2AR-/- mouse), lost their Th17-enhancing activity as did A2AR+/+ gammadelta
      T cells (isolated from wt-B6 mouse) after treatment with an A2AR antagonist.
      Since gammadelta T cells possess either an enhancing or an inhibiting effect, we 
      also tested whether A2AR expression on gammadelta T cells is essential to their
      inhibiting effect. Our results showed that the inhibiting effect of A2AR-/-
      gammadelta T cells was as potent as that of A2AR+/+ gammadelta T cells. In a
      previous report we showed that the expression of different levels of CD73
      molecule allowed gammadelta T cells to adjust their suppressive activity; in the 
      current study, we show that expression of increased amounts of A2AR allows
      gammadelta T cells to more effectively exert their enhancing function.
FAU - Liang, Dongchun
AU  - Liang D
AD  - Doheny Eye Institute and Department of Ophthalmology, David Geffen School of
      Medicine at UCLA, Los Angeles, CA, United States of America.
FAU - Shao, Hui
AU  - Shao H
AD  - Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center,
      University of Louisville, Louisville, Kentucky, United States of America.
FAU - Born, Willi K
AU  - Born WK
AD  - Department of Biomedical Research, National Jewish Health, Denver, CO, United
      States of America.
FAU - O'Brien, Rebecca L
AU  - O'Brien RL
AD  - Department of Biomedical Research, National Jewish Health, Denver, CO, United
      States of America.
FAU - Kaplan, Henry J
AU  - Kaplan HJ
AD  - Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center,
      University of Louisville, Louisville, Kentucky, United States of America.
FAU - Sun, Deming
AU  - Sun D
AUID- ORCID: 0000-0003-4851-0416
AD  - Doheny Eye Institute and Department of Ophthalmology, David Geffen School of
      Medicine at UCLA, Los Angeles, CA, United States of America.
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20180621
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Adora2a protein, mouse)
RN  - 0 (Receptor, Adenosine A2A)
RN  - 0 (Receptors, Antigen, T-Cell, gamma-delta)
SB  - IM
EIN - PLoS One. 2018 Nov 8;13(11):e0207546. PMID: 30408117
MH  - Animals
MH  - Autoimmune Diseases/*immunology
MH  - Autoimmunity/*physiology
MH  - Disease Models, Animal
MH  - Female
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Receptor, Adenosine A2A/genetics/*metabolism
MH  - Receptors, Antigen, T-Cell, gamma-delta/*immunology
MH  - Th17 Cells/immunology
MH  - Uveitis/*immunology
PMC - PMC6013223
COIS- The authors have declared that no competing interests exist.
EDAT- 2018/06/22 06:00
MHDA- 2019/01/01 06:00
CRDT- 2018/06/22 06:00
PHST- 2018/01/03 00:00 [received]
PHST- 2018/06/11 00:00 [accepted]
PHST- 2018/06/22 06:00 [entrez]
PHST- 2018/06/22 06:00 [pubmed]
PHST- 2019/01/01 06:00 [medline]
AID - 10.1371/journal.pone.0199601 [doi]
AID - PONE-D-18-00254 [pii]
PST - epublish
SO  - PLoS One. 2018 Jun 21;13(6):e0199601. doi: 10.1371/journal.pone.0199601.
      eCollection 2018.