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* Department of Pathology, Juntendo University School of Medicine, and
Department of Molecular Cell Immunology and Allergology, Advanced Medical Research Center, Nihon University School of Medicine, Tokyo, Japan;
Central Laboratory of First Clinical College, China Medical University, Shenyang, China;
Department of Pathology, Ehime University School of Medicine, Ehime, Japan; and
¶ Department of Experimental Immunology and Core Research for Engineering, Science, and Technology of Japan Science and Technology Corporation, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan
Fc
RIIB1 molecules serve as negative feedback regulator for B
cell Ag receptor-elicited activation of B cells; thus, any impaired
FcRIIB1 function may possibly be related to aberrant B cell
activation. We earlier found deletion polymorphism in the
Fcgr2b promoter region among mouse strains in which
systemic autoimmune disease-prone NZB, BXSB, MRL, and autoimmune
diabetes-prone nonobese diabetic, but not NZW, BALB/c, and
C57BL/6 mice have two identical deletion sites, consisting of 13 and 3
nucleotides. In this study, we established congenic C57BL/6 mice for
NZB-type Fcgr2b allele and found that NZB-type allele
down-regulates FcRIIB1 expression levels in germinal center B cells
and up-regulates IgG Ab responses. We did luciferase reporter assays to
determine whether NZB-type deletion polymorphism affects
transcriptional regulation of Fcgr2b gene. Although NZW-
and BALB/c-derived segments from position -302 to +585 of
Fcgr2b upstream region produced significant levels of
luciferase activities, only a limited activity was detected in the
NZB-derived sequence. EMSA and Southwestern analysis revealed that
defect in transcription activity in the NZB-derived segment is likely
due to absence of transactivation by AP-4, which binds to the
polymorphic 13 nucleotide deletion site. Our data imply that because of
the deficient AP-4 binding, the NZB-type Fcgr2b allele
polymorphism results in up-regulation of IgG Ab responses through
down-regulation of FcRIIB1 expression levels in germinal center B
cells, and that such polymorphism may possibly form the basis of
autoimmune susceptibility in combination with other background
contributing genes.
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