The contribution of macrophages to systemic lupus erythematosus.

The second most common clinical expression in lupus patients is skin damage that the pathogenesis remains unclear. We discuss the role of pathological factors in the development of skin damage in SLE. Skin deposited IgG is a crucial pathologic factor in the development of skin damage in SLE. Macrophages and signaling of TNFα/TNFR1 and IFN/IFNR play an important role in the skin injury of SLE. The intracellular molecules including Syk and calcium/calmodulin 4 and NFAT are involved in the manifestation of skin damage in lupus-prone mice. UV is the most typical environmental factor to trigger skin injury in areas of IgG deposition in SLE. These evidences indicate that skin deposited IgG is a crucial pathological factor to trigger skin lesions in SLE and blockade of IgG signaling may be effective target against skin injury of SLE.

/pdf/pathogenesis-of-skin-injury-of-systemic-lupus-erythematosus-4s1hs1uv3o.pdf

Pathogenesis of Skin Injury of Systemic Lupus Erythematosus.

Recent advances in cutaneous lupus.

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder characterized by high autoantibodies levels and multiorgan tissue damage. The current study investigated the role of CD64 in SLE patients and animal models. According to a flow cytometry study, SLE patients showed an increase in CD64 expression in circulating monocytes. There was a correlation between CD64 and SLEDAI, blood urea nitrogen levels, and anti-Sm antibodies. In skin lesions of lupus MRL/lpr mice, there was high IgG deposition and CD64 expression. In vitro, cytokines IL-10 and IFN-γ upregulated CD64 expression in monocytes/macrophages that was inhibited by glucocorticoids. In CD64-deficient mice, skin inflammation induced by lupus serum was reduced. Furthermore, activation of spleen tyrosine kinase (Syk), Akt, and extracellular signal-regulated kinase (Erk) was inhibited in CD64-deficient monocytes. The results suggest that CD64 could be a biomarker for observing SLE progression, as well as a mechanistic checkpoint in lupus pathogenesis.

/pdf/amelioration-of-lupus-serum-induced-skin-inflammation-in-1anzmxtg.pdf

Amelioration of Lupus Serum-Induced Skin Inflammation in CD64-Deficient Mice

Given the self-evident importance of cutaneous immunity in the maintenance of body-surface homeostasis, disturbance of the steady-state skin is inextricably intertwined with dysfunction in cutaneous immunity. It is often overlooked by people that skin, well-known as a solid physical barrier, is also a strong immunological barrier considering the abundant presence of immune cells including lymphocytes, granulocytes, dendritic cells and macrophages. What's more, humoral immune components including cytokines, immunoglobulins and antimicrobial peptides are also rich in the skin. This review will center around skin inflammation (acute and chronic, infection and aseptic inflammation), wound healing and skin cancer to elucidate the elaborate network of immune cells in skin diseases.

Immune cells in skin inflammation, wound healing and skin cancer.

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.

/pdf/the-role-of-estrogen-membrane-receptor-g-protein-coupled-5365y0u7il.pdf

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

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

The discovery of immunodominant antigens is of great significance for the development of new especially sensitive diagnostic reagents and effective vaccines in controlling tuberculosis (TB). In the present study, we targeted the T-Cell epitope-rich fragment (nucleotide position 109-552) of Rv1566c from Mycobacterium tuberculosis (MTB) and got a recombinant protein Rv1566c-444 and the full-length protein Rv1566c with Escherichia coli expression system, then compared their performances for TB diagnosis and immunogenicity in a mouse model. The results showed that Rv1566c-444 had similar sensitivity with Rv1566c (44.44% Vs 30.56%) but lower sensitivity than ESAT-6&CFP-10&Rv3615c (44.4% Vs. 94.4%) contained in a commercial kit for distinguishing TB patients from healthy donors. In immunized BALB/c mice, Rv1566c-444 elicited stronger T-helper 1 (Th1) cellular immune response over Rv1566c with higher levels of Th1 cytokine IFN-γ and IFN-γ/IL-4 expression ratio by ELISA; more importantly, with a higher proliferation of CD4+ T cells and a higher proportion of CD4+ TNF-α+ T cells with flow cytometry. Rv1566c-444 also induced a higher level of IL-6 by ELISA and a higher proportion of Rv1566c-444-specific CD8+ T cells and a lower proportion of CD8 + IL-4 + T cells by flow cytometry compared with the Rv1566c group. Moreover, the Rv1566c-444 group showed a high IgG secretion level and the same type of CD4+ Th cell immune response (both IgG1/IgG2a >1) as its parental protein group. Our results showed the potential of the recombinant protein Rv1566c-444 enriched with T-Cell epitopes from Rv1566c as a host T cell response measuring biomarker for TB diagnosis and support further evaluation of Rv1566c-444 as vaccine antigen against MTB challenge in animal models in the form of protein mixture or fusion protein.

/pdf/high-immunogenicity-of-a-t-cell-epitope-rich-recombinant-3aes1ll1.pdf

High Immunogenicity of a T-Cell Epitope-Rich Recombinant Protein Rv1566c-444 From Mycobacterium tuberculosis in Immunized BALB/c Mice, Despite Its Low Diagnostic Sensitivity

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

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

High Immunogenicity of a T-Cell Epitope-Rich Recombinant Protein Rv1566c-444 From Mycobacterium tuberculosis in Immunized BALB/c Mice, Despite Its Low Diagnostic Sensitivity