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Updated: Feb 17, 2026

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Immune complex negatively regulates toll-like receptor 3-triggered tumour necrosis factor α production in B cells
Li Qian1,2,3, Wenyan Chen1, Shaoqing Wang1
1Laboratory of Immunology, Yangzhou University School of Medicine, Yangzhou, China.
Abstract:
Inappropriate activation of toll-like receptor 3 (TLR3) has been implicated in the pathogenesis of autoimmune diseases, so the negative regulation of TLR3-triggered immune response has received increasing attention. Nonpathogenic immune complex (IC) has been used as treatment for many inflammatory and autoimmune diseases. However, the role of IC in the regulation of TLR3-triggered immune responses and the underlying mechanisms need to be investigated. In this study we demonstrate that IC or intravenous immunoglobulin (Ig) stimulation of B cells attenuates polyinosinic:polycytidylic acid (poly I:C)-induced CD40 expression; IC, but not Ig, can significantly inhibit poly I:C-induced pro-inflammatory tumour necrosis factor α (TNF-α) production by B cells. Moreover, IC/Ig stimulation does not alter the expression of TLR3 in B cells. Further experiments suggest that receptor for the Fc portion of IgGIIb (FcγRIIb) is involved in the suppressive effect of IC on TLR3-mediated TNF-α production, but not CD40 expression. Thus, we provide a new means of negative regulation of TLR3-triggered immune responses in B cells via FcγRIIb, and we provide a new mechanistic explanation of the therapeutic effect of nonpathogenic IC on inflammatory or autoimmune diseases.
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