PMID- 25522877
OWN - NLM
STAT- MEDLINE
DCOM- 20150313
LR  - 20141231
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 456
IP  - 2
DP  - 2015 Jan 9
TI  - Treatment of murine mast cells with IgEkappa and protein L enhances apoptotic cell 
      death induced by IL-3 withdrawal.
PG  - 700-5
LID - S0006-291X(14)02211-6 [pii]
LID - 10.1016/j.bbrc.2014.12.045 [doi]
AB  - Engagement of the high-affinity IgE receptor (FcepsilonRI) can be either protective or 
      non-protective against apoptotic cell death (ACD) in bone marrow-derived murine 
      mast cells (BMMCs) after IL-3 withdrawal, depending on the avidity between IgE 
      and its antigen. We recently reported that protein L (PpL), a bacterial 
      Igkappa-binding soluble protein, is able to stimulate intracellular signaling to 
      induce activation of BMMCs by interacting with the IgEkappa-FcepsilonRI complex. However, 
      it is unclear if cross-linking of FcepsilonRI with IgEkappa and PpL prevents or enhances 
      IL-3-dependent ACD in BMMCs. In the present study, we found that IL-3-dependent 
      ACD of BMMCs is accelerated by loading soluble PpL in the presence of 
      IgEkappa-occupied FcepsilonRIalpha. For this purpose, soluble PpL was incorporated into the 
      BMMCs. Unlike soluble PpL, immobilized PpL failed to enhance ACD, although both 
      forms of PpL induced IL-6 production equally in BMMCs. In addition, we observed 
      that DNS5-BSA protected anti-DNS IgE-sensitized BMMCs from IL-3 
      depletion-mediated ACD by inducing the production of autocrine IL-3. In contrast, 
      DNS5-PpL enhanced IL-3 withdrawal-induced ACD of anti-DNS IgE-sensitized BMMCs 
      and reduced the production of autocrine IL-3. These findings suggest that PpL 
      increases IL-3 withdrawal-induced ACD of IgEkappa-sensitized BMMCs by incorporating 
      PpL into the BMMCs and that this internalized PpL may interfere with survival 
      signals via FcepsilonRI.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Nunomura, Satoshi
AU  - Nunomura S
AD  - Department of Dermatology, Nihon University School of Medicine, Tokyo, Japan; 
      Allergy and Immunology Group, Research Institute of Medical Science, Nihon 
      University School of Medicine, Tokyo, Japan. Electronic address: 
      nunomura.satoshi@nihon-u.ac.jp.
FAU - Okayama, Yoshimichi
AU  - Okayama Y
AD  - Allergy and Immunology Group, Research Institute of Medical Science, Nihon 
      University School of Medicine, Tokyo, Japan.
FAU - Terui, Tadashi
AU  - Terui T
AD  - Department of Dermatology, Nihon University School of Medicine, Tokyo, Japan.
FAU - Ra, Chisei
AU  - Ra C
AD  - Allergy and Immunology Group, Research Institute of Medical Science, Nihon 
      University School of Medicine, Tokyo, Japan; Department of Microbiology, Nihon 
      University School of Medicine, Tokyo, Japan; Asahi Hospital, Chiba, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141215
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Bacterial Proteins)
RN  - 0 (Ig L-binding protein, Peptostreptococcus)
RN  - 0 (Immobilized Proteins)
RN  - 0 (Immunoglobulin kappa-Chains)
RN  - 0 (Interleukin-3)
RN  - 0 (Receptors, IgE)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/immunology/pharmacology
MH  - Apoptosis/drug effects/*immunology
MH  - Bacterial Proteins/*immunology/pharmacology
MH  - Cells, Cultured
MH  - Immobilized Proteins/immunology/pharmacology
MH  - Immunoglobulin E/*immunology
MH  - Immunoglobulin kappa-Chains/*immunology
MH  - Interleukin-3/*immunology
MH  - Mast Cells/drug effects/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Receptors, IgE/*immunology
OTO - NOTNLM
OT  - Cell death
OT  - IgE receptor
OT  - Mast cells
OT  - Protein L
OT  - Superantigen
EDAT- 2014/12/20 06:00
MHDA- 2015/03/17 06:00
CRDT- 2014/12/20 06:00
PHST- 2014/11/14 00:00 [received]
PHST- 2014/12/09 00:00 [accepted]
PHST- 2014/12/20 06:00 [entrez]
PHST- 2014/12/20 06:00 [pubmed]
PHST- 2015/03/17 06:00 [medline]
AID - S0006-291X(14)02211-6 [pii]
AID - 10.1016/j.bbrc.2014.12.045 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2015 Jan 9;456(2):700-5. doi: 
      10.1016/j.bbrc.2014.12.045. Epub 2014 Dec 15.