PMID- 11286538
OWN - NLM
STAT- MEDLINE
DCOM- 20010510
LR  - 20061115
IS  - 1521-6616 (Print)
IS  - 1521-6616 (Linking)
VI  - 99
IP  - 1
DP  - 2001 Apr
TI  - The B cell superantigen-like interaction of intravenous immunoglobin (IVIG) with 
      Fab fragments of V(H) 3-23 and 3-30/3-30.5 germline gene origin cloned from a 
      patient with Kawasaki disease is enhanced after IVIG therapy.
PG  - 18-29
AB  - The etiology of Kawasaki disease (KD) is still unknown. Therefore, the diagnosis 
      relies on clinical criteria only. Although a specific therapy for KD is not 
      available, coronary complications can be significantly reduced with the help of 
      intravenous immunoglobulin (IVIG) therapy. It is not clear how IVIG interacts 
      with the immune system. Previously, we selected a large number of IgG and IgM Fab 
      fragments specifically reacting with IVIG molecules by phage display and 
      antiidiotypic panning from three patients with autoimmune thrombocytopenia, a 
      patient with lupus, and a healthy individual. Sequencing revealed that the 
      favored V(H) germline gene segments of these IVIG-bound Fabs were 3-23 or 
      3-30/3-30.5, the most frequently rearranged V(H) genes among human B cells. The 
      binding pattern suggested a B cell superantigen-like, specific interaction of an 
      IVIG subset with B cells that present B cell receptors derived from these two 
      germline genes. The aim of the current study was to investigate whether treatment 
      with IVIG influences this restricted interaction. Therefore we cloned and 
      selected Fab fragments from a patient with KD before and after IVIG therapy. A 
      favored selection of antibodies derived from both the 3-23 and the 3-30/3-30.5 
      germline gene segments as before was observed. Importantly, the reactivity with 
      IVIG was significantly higher for clones from the library prepared after the IVIG 
      treatment, providing the first in vivo functional evidence that a subset of IVIG 
      may selectively activate B cells of this germline origin. This mechanism may add 
      to the therapeutic effect of IVIG in the treatment of KD.
CI  - Copyright 2001 Academic Press.
FAU - Leucht, S
AU  - Leucht S
AD  - Laboratory of Molecular Biology, Children's Hospital, Otto Heubner Centrum, 
      Charite, Humboldt-University, 10117 Berlin, Germany.
FAU - Uttenreuther-Fischer, M M
AU  - Uttenreuther-Fischer MM
FAU - Gaedicke, G
AU  - Gaedicke G
FAU - Fischer, P
AU  - Fischer P
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Clin Immunol
JT  - Clinical immunology (Orlando, Fla.)
JID - 100883537
RN  - 0 (Immunoglobulin Fab Fragments)
RN  - 0 (Immunoglobulin Heavy Chains)
RN  - 0 (Immunoglobulin Light Chains)
RN  - 0 (Immunoglobulin Variable Region)
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Peptide Library)
RN  - 0 (Superantigens)
SB  - IM
MH  - B-Lymphocytes/*immunology
MH  - Child, Preschool
MH  - Female
MH  - Humans
MH  - Immunoglobulin Fab Fragments/*genetics
MH  - Immunoglobulin Heavy Chains/*genetics
MH  - Immunoglobulin Light Chains/genetics
MH  - Immunoglobulin Variable Region/*genetics
MH  - Immunoglobulins, Intravenous/immunology/*therapeutic use
MH  - Mucocutaneous Lymph Node Syndrome/immunology/*therapy
MH  - Peptide Library
MH  - Superantigens/*immunology
EDAT- 2001/04/05 10:00
MHDA- 2001/05/22 10:01
CRDT- 2001/04/05 10:00
PHST- 2001/04/05 10:00 [pubmed]
PHST- 2001/05/22 10:01 [medline]
PHST- 2001/04/05 10:00 [entrez]
AID - S1521-6616(01)95004-1 [pii]
AID - 10.1006/clim.2001.5004 [doi]
PST - ppublish
SO  - Clin Immunol. 2001 Apr;99(1):18-29. doi: 10.1006/clim.2001.5004.