PMID- 26049110
OWN - NLM
STAT- MEDLINE
DCOM- 20151102
LR  - 20150708
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 463
IP  - 4
DP  - 2015 Aug 7
TI  - ICOS promotes group 2 innate lymphoid cell activation in lungs.
PG  - 739-45
LID - S0006-291X(15)30058-9 [pii]
LID - 10.1016/j.bbrc.2015.06.005 [doi]
AB  - Group 2 innate lymphoid cells (ILC2s) are newly identified, potent producers of 
      type 2 cytokines, such as IL-5 and IL-13, and contribute to the development of 
      allergic lung inflammation induced by cysteine proteases. Although it has been 
      shown that inducible costimulator (ICOS), a costimulatory molecule, is expressed 
      on ILC2s, the role of ICOS in ILC2 responses is largely unknown. In the present 
      study, we investigated whether the interaction of ICOS with its ligand B7-related 
      protein-1 (B7RP-1) can promote ILC2 activation. Cytokine production in ILC2s 
      purified from mouse lungs was significantly increased by coculture with 
      B7RP-1-transfected cells, and increased cytokine production was inhibited by 
      monoclonal antibody-mediated blocking of the ICOS/B7RP-1 interaction. ILC2 
      expansion and eosinophil influx induced by papain, a cysteine protease antigen, 
      in mouse lungs were significantly abrogated by blocking the ICOS/B7RP-1 
      interaction. Dendritic cells (DCs) in the lungs expressed B7RP-1 and the number 
      of DCs markedly increased with papain administration. B7RP-1 expression on lung 
      DCs was reduced after papain administration. This downregulation of B7RP-1 
      expression may be an indication of ICOS/B7RP-1 binding. These results indicate 
      that ILC2s might interact with B7RP-1-expressing DCs in allergic inflammatory 
      lung, and ICOS signaling can positively regulate the protease allergen-induced 
      ILC2 activation followed by eosinophil infiltration into the lungs.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Kamachi, Fumitaka
AU  - Kamachi F
AD  - Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, 
      Bunkyo-ku, Tokyo 113-8421, Japan. Electronic address: fkamachi@juntendo.ac.jp.
FAU - Isshiki, Takuma
AU  - Isshiki T
AD  - Division of Respiratory Medicine, Toho University Omori Medical Center, 6-11-1, 
      Omori-nishi, Ota-ku, Tokyo 143-8541, Japan.
FAU - Harada, Norihiro
AU  - Harada N
AD  - Department of Respiratory Medicine, Juntendo University School of Medicine, 2-1-1 
      Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
FAU - Akiba, Hisaya
AU  - Akiba H
AD  - Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, 
      Bunkyo-ku, Tokyo 113-8421, Japan.
FAU - Miyake, Sachiko
AU  - Miyake S
AD  - Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, 
      Bunkyo-ku, Tokyo 113-8421, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150604
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Inducible T-Cell Co-Stimulator Protein)
RN  - EC 3.4.22.2 (Papain)
SB  - IM
MH  - Animals
MH  - Flow Cytometry
MH  - Immunity, Innate/*immunology
MH  - Inducible T-Cell Co-Stimulator Protein/*physiology
MH  - Lung/drug effects/*immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Papain/pharmacology
OTO - NOTNLM
OT  - Allergic lung inflammation
OT  - Group 2 innate lymphoid cell
OT  - Inducible costimulator
EDAT- 2015/06/07 06:00
MHDA- 2015/11/03 06:00
CRDT- 2015/06/07 06:00
PHST- 2015/05/16 00:00 [received]
PHST- 2015/06/02 00:00 [accepted]
PHST- 2015/06/07 06:00 [entrez]
PHST- 2015/06/07 06:00 [pubmed]
PHST- 2015/11/03 06:00 [medline]
AID - S0006-291X(15)30058-9 [pii]
AID - 10.1016/j.bbrc.2015.06.005 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2015 Aug 7;463(4):739-45. doi: 
      10.1016/j.bbrc.2015.06.005. Epub 2015 Jun 4.