Journal
JOURNAL OF GASTROENTEROLOGY
Volume 48, Issue 2, Pages 247-253Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s00535-012-0626-8
Keywords
IgG4-related disease; Basophil; TLR
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Funding
- Ministry of Education, Science and Culture, Japan
- Japan Society for the Promotion of Science [21590532]
- Takeda Science Foundation
- Astellas Foundation for Research on Metabolic Disorders
- Yakult Bioscience Foundation
- Cell Science Research Foundation
- Kato Memorial Trust for Nambyo Research
- Pancreas Research Foundation of Japan
- Uehara Memorial Foundation
- Health and Labour Sciences Research Grants for research on intractable diseases from the Ministry of Health, Labour and Welfare of Japan
- Grants-in-Aid for Scientific Research [23590998, 21590532, 24591020] Funding Source: KAKEN
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IgG4-related disease (IRD) is characterized by systemic IgG4 antibody responses and by infiltration of IgG4-expressing plasma cells into the affected organs. Although T helper type 2 (Th2) cytokines are implicated in enhanced IgG4 responses, molecular mechanisms accounting for the development of IgG4 antibody responses are poorly defined. Since basophils function as antigen-presenting cells for Th2 responses, we tried to clarify the role of basophils in the development of IgG4 responses in this study. IgG4 and cytokine responses to various nucleotide-binding oligomerization domain-like receptor and Toll-like receptor (TLR) ligands were examined by using basophils isolated from healthy controls and from patients with IgG4-related disease. Activation of TLRs in basophils from healthy controls induced IgG4 production by B cells, which effect was associated with enhanced production of B cell activating factor (BAFF) and IL-13. In addition, activation of TLRs in basophils from patients with IRD induced a large amount of IgG4 by B cells from healthy controls. This enhancement of IgG4 production was again associated with BAFF and IL-13. These data suggest that innate immune responses mediated through TLRs may play a role in the development of IgG4-related disease, in part by production of BAFF from basophils.
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