PMID- 28458281
OWN - NLM
STAT- MEDLINE
DCOM- 20170810
LR  - 20211204
IS  - 1347-5231 (Electronic)
IS  - 0031-6903 (Linking)
VI  - 137
IP  - 5
DP  - 2017
TI  - [Role of Histamine-releasing Factor in Allergic Inflammatory Reactions].
PG  - 517-521
LID - 10.1248/yakushi.16-00239-3 [doi]
AB  - Mast cells are effector cells in immunoglobulin E (IgE)-mediated immediate 
      hypersensitivity and allergic diseases such as asthma and food allergy. Mast 
      cells are activated by the aggregation of the IgE-bound high-affinity IgE 
      receptor FcepsilonRI with multivalent antigen. Activated mast cells secrete 
      proinflammatory mediators such as histamine, serotonin, and proteases and produce 
      cytokines and chemokines. However, it has been reported that mast cells are 
      activated by crosslinking of FcepsilonRI with monomeric IgE in the absence of antigen. 
      We have recently demonstrated that histamine-releasing factor (HRF) is involved 
      in IgE-mediated mast cell activation both in vitro and in vivo. HRF binds to a 
      subset of IgE and IgG molecules [HRF-reactive antibodies (Abs)]. The Fab, but not 
      Fc, portions of the IgE and IgG molecules are HRF-binding sites, and the 
      N-terminal 19-residue (N19) and H3 portions of HRF are HRF-reactive Ab-binding 
      sites. We observed that both N19 and H3 tagged with glutathione S transferase 
      (GST) (GST-N19 and GST-H3) can inhibit the interaction between HRF and 
      HRF-reactive Abs. Using acute- and late-phase passive cutaneous anaphylaxis mouse 
      models, it was shown that HRF initiates mast cell activation through 
      HRF-reactive, but not HRF-nonreactive, IgE in vivo. Antigen-induced passive 
      cutaneous anaphylaxis was inhibited by pretreatment with GST-N19 and GST-H3. We 
      demonstrated that pretreatment with GST-N19 before antigen challenge inhibited 
      antigen-induced mast cell-dependent airway inflammation. In addition, GST-N19 
      partially inhibited Aspergillus fumigatus extract-induced IgE-dependent airway 
      inflammation. However, GST-N19 did not inhibit T cell-dependent airway 
      inflammation. These results suggest that mast cells are target cells for HRF to 
      initiate IgE- and mast cell-dependent airway inflammation.
FAU - Kashiwakura, Jun-Ichi
AU  - Kashiwakura JI
AD  - Laboratory for Allergic Disease, RIKEN Center for Integrative Medical Sciences.
AD  - Allergy and Immunology Project Team, Division of Medical Education Planning and 
      Development, Nihon University School of Medicine.
AD  - Division of Cell Biology, La Jolla Institute for Allergy and Immunology.
FAU - Ando, Tomoaki
AU  - Ando T
AD  - Laboratory for Allergic Disease, RIKEN Center for Integrative Medical Sciences.
FAU - Kawakami, Toshiaki
AU  - Kawakami T
AD  - Laboratory for Allergic Disease, RIKEN Center for Integrative Medical Sciences.
AD  - Division of Cell Biology, La Jolla Institute for Allergy and Immunology.
LA  - jpn
PT  - Journal Article
PT  - Review
PL  - Japan
TA  - Yakugaku Zasshi
JT  - Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
JID - 0413613
RN  - 0 (Antibodies)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Tumor Protein, Translationally-Controlled 1)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - EC 2.5.1.18 (Glutathione Transferase)
SB  - IM
MH  - Animals
MH  - Antibodies/immunology/metabolism
MH  - Asthma/*immunology
MH  - Binding Sites
MH  - Biomarkers, Tumor/immunology/metabolism/*physiology
MH  - Glutathione Transferase/immunology/metabolism
MH  - Humans
MH  - Immunoglobulin E/immunology/metabolism
MH  - Mast Cells/*immunology
MH  - Mice
MH  - Passive Cutaneous Anaphylaxis/immunology
MH  - Protein Binding
MH  - Tumor Protein, Translationally-Controlled 1
OTO - NOTNLM
OT  - asthma
OT  - histamine-releasing factor
OT  - immunoglobulin E
OT  - mast cell
EDAT- 2017/05/02 06:00
MHDA- 2017/08/11 06:00
CRDT- 2017/05/02 06:00
PHST- 2017/05/02 06:00 [entrez]
PHST- 2017/05/02 06:00 [pubmed]
PHST- 2017/08/11 06:00 [medline]
AID - 10.1248/yakushi.16-00239-3 [doi]
PST - ppublish
SO  - Yakugaku Zasshi. 2017;137(5):517-521. doi: 10.1248/yakushi.16-00239-3.