PMID- 15572393
OWN - NLM
STAT- MEDLINE
DCOM- 20050412
LR  - 20171116
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 44
IP  - 3
DP  - 2005 Mar
TI  - Intravenous immunoglobulin does not increase FcgammaRIIB expression on 
      monocytes/macrophages during acute Kawasaki disease.
PG  - 314-7
AB  - OBJECTIVES: Intravenous immunoglobulin (IVIG) therapy has been reported to be 
      effective for reducing the incidence of coronary artery lesions in Kawasaki 
      disease (KD), an acute febrile vasculitis of unknown aetiology. Regarding the 
      mechanism of IVIG in immune thrombocytopenic purpura (ITP), it has been reported 
      that IVIG increases the expression of the inhibitory Fc receptor, FcgammaRIIB 
      (CD32B), on splenic macrophages in a murine ITP model. Regarding the mechanism of 
      IVIG during acute KD, we investigated whether or not IVIG increases the 
      expression of FcgammaRIIB in peripheral blood CD14+ monocytes/macrophages. 
      METHODS: The expression of FcgammaRIIB in peripheral blood CD14+ 
      monocytes/macrophages was determined before and after IVIG therapy in 13 patients 
      with acute KD by flow cytometry. RESULTS: The percentage of CD14+ CD32B+ 
      monocytes/macrophages among peripheral blood mononuclear cells, the absolute 
      number of CD14+ CD32B+ monocytes/macrophages and the percentage of CD14+ CD32B+ 
      monocytes/macrophages among CD14+ monocytes/macrophages in patients with acute KD 
      before IVIG therapy were significantly increased compared with those after IVIG 
      therapy and in controls. CD14+ CD32B+ monocytes/macrophages decreased to within 
      the normal range soon after IVIG therapy. CONCLUSIONS: IVIG therapy in patients 
      with KD did not increase the expression of FcgammaRIIB in peripheral blood CD14+ 
      monocytes/macrophages during the acute stage.
FAU - Ichiyama, T
AU  - Ichiyama T
AD  - Department of Pediatrics, Yamaguchi University School of Medicine, 1-1-1 
      Minami-kogushi, Ube, Yamaguchi 755-8505, Japan. ichiyama@yamaguchi-u.ac.jp
FAU - Ueno, Y
AU  - Ueno Y
FAU - Hasegawa, M
AU  - Hasegawa M
FAU - Ishikawa, Y
AU  - Ishikawa Y
FAU - Matsubara, T
AU  - Matsubara T
FAU - Furukawa, S
AU  - Furukawa S
LA  - eng
PT  - Journal Article
DEP - 20041130
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Antigens, CD)
RN  - 0 (Fc gamma receptor IIB)
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (Receptors, IgG)
SB  - IM
EIN - Rheumatology (Oxford). 2005 Apr;44(4):569
MH  - Acute Disease
MH  - Antigens, CD/*blood
MH  - Child, Preschool
MH  - Female
MH  - Humans
MH  - Immunoglobulins, Intravenous/*therapeutic use
MH  - Infant
MH  - Lipopolysaccharide Receptors/immunology
MH  - Macrophages/*immunology
MH  - Male
MH  - Monocytes/*immunology
MH  - Mucocutaneous Lymph Node Syndrome/immunology/*therapy
MH  - Receptors, IgG/*blood/immunology
EDAT- 2004/12/02 09:00
MHDA- 2005/04/13 09:00
CRDT- 2004/12/02 09:00
PHST- 2004/12/02 09:00 [pubmed]
PHST- 2005/04/13 09:00 [medline]
PHST- 2004/12/02 09:00 [entrez]
AID - keh488 [pii]
AID - 10.1093/rheumatology/keh488 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2005 Mar;44(3):314-7. doi: 10.1093/rheumatology/keh488. 
      Epub 2004 Nov 30.