PMID- 18714538
OWN - NLM
STAT- MEDLINE
DCOM- 20081006
LR  - 20171116
IS  - 1018-9068 (Print)
IS  - 1018-9068 (Linking)
VI  - 18
IP  - 4
DP  - 2008
TI  - Activation of basophils by stem cell factor: comparison with insulin-like growth 
      factor-I.
PG  - 293-9
AB  - BACKGROUND: Basophils are an active participant in the pathogenesis of local 
      inflammation in allergic diseases such as asthma, but it is not fully known how 
      basophil activation is regulated in inflamed tissue. OBJECTIVE: In order to 
      clarify the control mechanisms of basophil activation in chronic inflammation and 
      at remodeling sites, we analyzed the effects of fibroblast-derived cytokines, 
      stem cell factor (SCF), and insulin-like growth factor-I (IGF-I) on basophils. 
      METHODS: The effects of SCF and IGF-I on degranulation and surface activation 
      marker expression by basophils were assessed and compared. RESULTS: SCF enhanced 
      human basophil histamine release elicited by some, but not all, secretagogues; 
      degranulation in response to IgE- or FcepsilonRI-mediated stimulation and 
      12-o-tetradecanoyl-phorbol-13-acetate (TPA) was enhanced by SCF. SCF slightly 
      enhanced ionophore A23187-induced histamine release by basophils from some 
      donors, but it failed to affect the release elicited by monocyte chemoattractant 
      protein-1 (MCP-1), formylmethionyl-leucyl-phenylalanine (FMLP) or C5a. The 
      repertoire of secretagogues responsive to SCF was similar to that of IGF-I. 
      Expression levels of both CD11b and CD69 markers were significantly enhanced by 
      the combination of SCF and IGF-I. CONCLUSIONS: These results suggest that SCF and 
      IGF-I may modify the activation of basophils in a similar and/or synergistic 
      fashion. Interaction of basophils with these cytokines might be involved in the 
      pathogenesis of local inflammation and the remodeling process in asthma.
FAU - Koketsu, R
AU  - Koketsu R
AD  - Department of Allergy and Rheumatology, University of Tokyo Graduate School of 
      Medicine, Tokyo, Japan.
FAU - Suzukawa, M
AU  - Suzukawa M
FAU - Kawakami, A
AU  - Kawakami A
FAU - Komiya, A
AU  - Komiya A
FAU - Ra, C
AU  - Ra C
FAU - Yamamoto, K
AU  - Yamamoto K
FAU - Yamaguchi, M
AU  - Yamaguchi M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Spain
TA  - J Investig Allergol Clin Immunol
JT  - Journal of investigational allergology & clinical immunology
JID - 9107858
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, T-Lymphocyte)
RN  - 0 (CD11b Antigen)
RN  - 0 (CD69 antigen)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Stem Cell Factor)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
SB  - IM
MH  - Antigens, CD/immunology/*metabolism
MH  - Antigens, Differentiation, T-Lymphocyte/immunology/*metabolism
MH  - Basophils/drug effects/*immunology/metabolism
MH  - CD11b Antigen/drug effects/immunology/*metabolism
MH  - Cell Degranulation/*drug effects
MH  - Histamine Release/*drug effects
MH  - Humans
MH  - Insulin-Like Growth Factor I/immunology/*pharmacology
MH  - Lectins, C-Type
MH  - Recombinant Proteins/pharmacology
MH  - Stem Cell Factor/immunology/*pharmacology
EDAT- 2008/08/22 09:00
MHDA- 2008/10/07 09:00
CRDT- 2008/08/22 09:00
PHST- 2008/08/22 09:00 [pubmed]
PHST- 2008/10/07 09:00 [medline]
PHST- 2008/08/22 09:00 [entrez]
PST - ppublish
SO  - J Investig Allergol Clin Immunol. 2008;18(4):293-9.