Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by dysfunction of T cells, B cells, and antigen-presenting cells. A number of cytokine network abnormalities have been reported in patients with SLE and in lupus model mice. Some of them play an important physiological role in the development of the disease, while others are considered bystanders. For example, B-cell activators regulate B-cell maturation and survival, and their imbalance is associated with systemic autoimmunity in SLE and lupus nephritis. Recently, type I interferons (IFNs) and IFN signaling (mainly IFNa and IFNß) have also been implicated in the pathogenesis of SLE and have been shown to play an important cytokine role in lupus. It is thought to be involved in a variety of pathological conditions in SLE, but the details are still unknown.
The aim of this Research Topic is to stimulate active discussion among researchers from around the world on topics such as cytokine transmission pathways and novel therapeutic strategies in the pathophysiology of systemic lupus erythematosus (SLE). The aim is to advance the field of SLE research and improve the care of patients with this complex and challenging disease by facilitating discussion and presenting research findings.
Therefore, we welcome the submission of articles that cover, but are not limited to, the following sub-topics:
• Cytokine signaling pathways in SLE
• Novel SLE therapeutic strategies in the suppression of B-cell activation and type I IFN activity
• Effects of inflammatory cytokines on the pathogenesis in SLE
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by dysfunction of T cells, B cells, and antigen-presenting cells. A number of cytokine network abnormalities have been reported in patients with SLE and in lupus model mice. Some of them play an important physiological role in the development of the disease, while others are considered bystanders. For example, B-cell activators regulate B-cell maturation and survival, and their imbalance is associated with systemic autoimmunity in SLE and lupus nephritis. Recently, type I interferons (IFNs) and IFN signaling (mainly IFNa and IFNß) have also been implicated in the pathogenesis of SLE and have been shown to play an important cytokine role in lupus. It is thought to be involved in a variety of pathological conditions in SLE, but the details are still unknown.
The aim of this Research Topic is to stimulate active discussion among researchers from around the world on topics such as cytokine transmission pathways and novel therapeutic strategies in the pathophysiology of systemic lupus erythematosus (SLE). The aim is to advance the field of SLE research and improve the care of patients with this complex and challenging disease by facilitating discussion and presenting research findings.
Therefore, we welcome the submission of articles that cover, but are not limited to, the following sub-topics:
• Cytokine signaling pathways in SLE
• Novel SLE therapeutic strategies in the suppression of B-cell activation and type I IFN activity
• Effects of inflammatory cytokines on the pathogenesis in SLE