Abstract
The hallmarks of IgG4-related disease (IgG4-RD) are lymphoplasmacytic tissue infiltration with a predominance of IgG4-positive plasma cells, accompanied by fibrosis, obliterative phlebitis, dacryoadenitis, and elevated levels of IgG4. In a recent issue of Arthritis Research & Therapy, Tsuboi and colleagues demonstrated that regulatory T (Treg) cell-and T helper 2 (Th2) cell-derived cytokines contribute to the pathogenesis of Mikulicz's disease, an activation pathway that appears to be common for IgG4-RD. Additional organ-specific factors may account for the different organ involvement of IgG4-RD.
Highlights
The hallmarks of IgG4-related disease (IgG4-RD) are lymphoplasmacytic tissue infiltration with a predominance of IgG4-positive plasma cells, accompanied by fibrosis, obliterative phlebitis, dacryoadenitis, and elevated levels of IgG4
The authors provided evidence that IL-10, transforming growth factor-beta (TGF-β), and activationinduced cytidine deaminase (AID) were overexpressed in labial salivary gland (LSG) from IgG4-RD (MD) compared with those in patients with s syndrome (SS), suggesting that regulatory T (Treg) cytokines (IL-10 and TGF-β) contribute to IgG4-specifc class switch recombination and fibrosis in patients with IgG4-RD (MD) in combination with the IgG4-unrelated molecule, AID (Figure 1)
The authors showed that the levels of mRNA for both T helper 2 (Th2) and Treg cytokines were significantly higher in LSGs from patients with IgG4-RD (MD) but that the expressions of Th1 and Th2 cytokines were higher in LSGs from patients with SS
Summary
The hallmarks of IgG4-related disease (IgG4-RD) are lymphoplasmacytic tissue infiltration with a predominance of IgG4-positive plasma cells, accompanied by fibrosis, obliterative phlebitis, dacryoadenitis, and elevated levels of IgG4. In a recent issue of Arthritis Research & Therapy, Tsuboi and colleagues [5] analyzed the expression of IgG4-specific class switch molecules such as Th2 cytokines (IL-4 and IL-13) and Treg cytokines (IL-10 and TGF-β), IgG4-nonspecific B cell regulatory molecules (CD40, CD154, BAFF, APRIL, and IRF4), and activationinduced cytidine deaminase (AID) in the labial salivary glands (LSGs) and peripheral blood mononuclear cells (PBMCs) from patients with IgG4-RD (MD) and SS.
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