Corrigendum: The Role of Estrogen Membrane Receptor (G Protein-Coupled Estrogen Receptor 1) in Skin Inflammation Induced by Systemic Lupus Erythematosus Serum IgG.

[This corrects the article DOI: 10.3389/fimmu.2017.01723.].

The role of neutrophils in skin damage induced by tissue-deposited lupus IgG.

Skin injury is the second most common clinical manifestation in patients with systemic lupus erythematosus (SLE). Neutrophils are crucial effector cells in the immune system but the significance of neutrophils in the pathogenesis of SLE is not clear. This study is to explore the role of neutrophils in the skin damage of SLE. We used lupus-prone mice and a C57BL/6 mouse model of lupus serum IgG-induced skin inflammation to investigate the role of neutrophils in skin damage of SLE. We found that a few neutrophils infiltrated the inflammatory sites of skin in lupus-prone mice and the lupus-IgG-induced skin damage mouse model. Depletion of neutrophils did not affect the development of skin inflammation caused by lupus IgG, and lupus IgG can induce apoptosis of neutrophils. The apoptosis of neutrophils induced by lupus IgG is related to FcγRIII and Fas/Fas ligand pathways. Our study indicates that neutrophils are not major contributors in the skin damage caused by tissue-deposited lupus IgG but death of neutrophils caused by lupus IgG may provide a resource of a large amount of autoantigens in SLE.

The Role of Estrogen Membrane Receptor (G Protein-Coupled Estrogen Receptor 1) in Skin Inflammation Induced by Systemic Lupus Erythematosus Serum IgG.

Skin injury is the second most common clinical manifestation in patients with systemic lupus erythematosus (SLE). Estrogen may affect the onset and development of SLE through its receptor. In this study, we investigated the role of estrogen membrane receptor G protein-coupled estrogen receptor 1 (GPER1) in skin injury of SLE. We found that skin injury induced by SLE serum was more severe in female mice and required monocytes. Estrogen promoted activation of monocytes induced by lupus IgG through the membrane receptor GPER1 which was located in lipid rafts. Blockade of GPER1 and lipid rafts reduced skin inflammation induced by SLE serum. The results we obtained suggest that GPER1 plays an important role in the pathogenesis of skin inflammation induced by lupus IgG and might be a therapeutic target in skin lesions of patients with SLE.

Skin inflammation induced by lupus serum was inhibited in IL-1R deficient mice.

Skin inflammation induced by lupus serum is a useful tool to investigate the pathogenesis of lupus skin injury. IL-1 is a proinflammatory cytokine, and its role in lupus skin lesion is still unclear. We determined the role of IL-1 in lupus skin injury by using gene deficient mice. We found that skin inflammation induced by lupus serum was significantly reduced in IL-1R deficient mice and caspase-1 deficient mice. IL-1R deficiency did not affect the expression of FcγRI (CD64), FcγRII (CD32) and MHC class II (CD74) induced by lupus serum. IL-1R deficiency reduced the lipid raft clustering, and decreased expression of MCP-1 and TNFα in monocytes. Keratinocyte proliferation induced by lupus serum was significantly decreased in TNFα deficient mice. Our findings indicate that IL-1 plays an important role in skin lesions of SLE. This study suggests that IL-1 is a therapeutic target in skin lesions of SLE.