PMID- 28675838
OWN - NLM
STAT- MEDLINE
DCOM- 20180221
LR  - 20180221
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 50
DP  - 2017 Sep
TI  - Therapeutic application of human leukocyte antigen-G1 improves atopic 
      dermatitis-like skin lesions in mice.
PG  - 202-207
LID - S1567-5769(17)30256-4 [pii]
LID - 10.1016/j.intimp.2017.06.026 [doi]
AB  - Human leukocyte antigen (HLA)-G is an immune checkpoint molecule that plays 
      critical roles in immune response and in triggering inhibitory signaling to 
      immune cells such as T cells, natural killer cells, and antigen-presenting cells. 
      Thus, the application of HLA-G can be considered for treating immune 
      response-related inflammatory disorders. We have previously reported that 
      treatment with HLA-G1 and HLA-G2 ameliorates the joint swelling associated with 
      collagen-induced arthritis of DBA/1 mice, an animal model for rheumatoid 
      arthritis. In this study, we further investigated the effects of HLA-G1 on atopic 
      dermatitis (AD), the most common inflammatory skin disorder. AD-like lesions were 
      induced with the extract of the house dust mite Dermatophagoides farinae in 
      NC/Nga mice. Continuous administration of HLA-G1 ameliorated the AD-like skin 
      lesions in the mice. Furthermore, production of immunoglobulin E, interleukin 
      (IL)-13, and IL-17A was significantly reduced in HLA-G1-treated mice, suggesting 
      a Th2/Th17-mediated immune-inhibitory function of HLA-G1 in vivo. Our studies 
      shed light on novel therapeutic strategies with recombinant HLA-G proteins for 
      immune reaction-mediated chronic inflammatory disorders.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Maeda, Naoyoshi
AU  - Maeda N
AD  - Center for Research and Education on Drug Discovery, Faculty of Pharmaceutical 
      Sciences, Hokkaido University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, 
      Japan.
FAU - Yamada, Chisato
AU  - Yamada C
AD  - Laboratory of Biomolecular Science, Faculty of Pharmaceutical Sciences, Hokkaido 
      University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, Japan.
FAU - Takahashi, Ami
AU  - Takahashi A
AD  - Laboratory of Biomolecular Science, Faculty of Pharmaceutical Sciences, Hokkaido 
      University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, Japan.
FAU - Kuroki, Kimiko
AU  - Kuroki K
AD  - Laboratory of Biomolecular Science, Faculty of Pharmaceutical Sciences, Hokkaido 
      University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, Japan. Electronic 
      address: k-kuroki@pharm.hokudai.ac.jp.
FAU - Maenaka, Katsumi
AU  - Maenaka K
AD  - Center for Research and Education on Drug Discovery, Faculty of Pharmaceutical 
      Sciences, Hokkaido University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, 
      Japan; Laboratory of Biomolecular Science, Faculty of Pharmaceutical Sciences, 
      Hokkaido University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, Japan. 
      Electronic address: maenaka@pharm.hokudai.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20170701
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Antigens, Dermatophagoides)
RN  - 0 (HLA-G Antigens)
RN  - 0 (Interleukin-13)
RN  - 0 (Interleukin-17)
RN  - 0 (Protein Isoforms)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Antigens, Dermatophagoides/immunology
MH  - Dermatitis, Atopic/immunology/*therapy
MH  - Dermatophagoides farinae/immunology
MH  - Disease Models, Animal
MH  - Female
MH  - HLA-G Antigens/*therapeutic use
MH  - Humans
MH  - Immunoglobulin E/blood
MH  - Immunotherapy/*methods
MH  - Interleukin-13/metabolism
MH  - Interleukin-17/metabolism
MH  - Mice
MH  - Mice, Inbred DBA
MH  - Protein Isoforms
MH  - Skin/*immunology/pathology
MH  - Th2 Cells/*immunology
OTO - NOTNLM
OT  - Atopic dermatitis
OT  - Dermatophagoides farinae
OT  - HLA-G1
OT  - NC/Nga mice
EDAT- 2017/07/05 06:00
MHDA- 2018/02/22 06:00
CRDT- 2017/07/05 06:00
PHST- 2017/01/29 00:00 [received]
PHST- 2017/06/22 00:00 [revised]
PHST- 2017/06/23 00:00 [accepted]
PHST- 2017/07/05 06:00 [pubmed]
PHST- 2018/02/22 06:00 [medline]
PHST- 2017/07/05 06:00 [entrez]
AID - S1567-5769(17)30256-4 [pii]
AID - 10.1016/j.intimp.2017.06.026 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2017 Sep;50:202-207. doi: 10.1016/j.intimp.2017.06.026. Epub 
      2017 Jul 1.