Lupus is a group of heterogeneous autoimmune diseases with multiple organ involvement. Type I interferons (IFNs) are drivers of lupus, and their role in clinical manifestations of the disease is apparent with the recent approval of anifrolumab, a first-in-class type I interferon receptor antibody and the only new medicine in over a decade for patients with systemic lupus erythematosus (SLE). However, to date, the majority of research studies have focused on the role of a limited number of type I IFNs, namely IFNa and IFNk.
In addition to type I IFNs, multiple other pro-inflammatory cytokines are important in the pathophysiology of SLE including several that impact the differentiation and proliferation of B cells (e.g., BAFF (the target of belimumab), IL-21, IL-10) or T cells (e.g. IL-2, IL-17, IL-23). Also many chemokines are involved in the migration of multiple cell types such as CCL2, CCL-3-5, and CXCL-10. However, more remains to be understood about these and other factors in not only SLE but also lupus nephritis (LN), cutaneous lupus (CLE) and neuropsychiatric aspects of SLE.
Goal of this Research Topic is to understand how IFN family members and other proinflammatory mediators are associated with specific lupus clinical phenotypes or disease endotypes.
In this article collection, we aim to include manuscripts that describe the role of interferons and other proinflammatory mediators in lupus including but not limited to: skin, vasculature, kidney, CNS. These studies may describe insights into IFN family members as well as the interplay and networks of established and more novel proinflammatory cytokines and their receptors.
Guest Editors declaration:
1. WIW is an employee of AstraZeneca and owns stock in AstraZeneca.
2. JMR is an inventor on use patents filed for “Diagnosis of skin conditions in veterinary and human patients”, and for targeting CXCR3 (0#15/851,651) and IL15 (# 62489191) for the treatment of vitiligo.
Lupus is a group of heterogeneous autoimmune diseases with multiple organ involvement. Type I interferons (IFNs) are drivers of lupus, and their role in clinical manifestations of the disease is apparent with the recent approval of anifrolumab, a first-in-class type I interferon receptor antibody and the only new medicine in over a decade for patients with systemic lupus erythematosus (SLE). However, to date, the majority of research studies have focused on the role of a limited number of type I IFNs, namely IFNa and IFNk.
In addition to type I IFNs, multiple other pro-inflammatory cytokines are important in the pathophysiology of SLE including several that impact the differentiation and proliferation of B cells (e.g., BAFF (the target of belimumab), IL-21, IL-10) or T cells (e.g. IL-2, IL-17, IL-23). Also many chemokines are involved in the migration of multiple cell types such as CCL2, CCL-3-5, and CXCL-10. However, more remains to be understood about these and other factors in not only SLE but also lupus nephritis (LN), cutaneous lupus (CLE) and neuropsychiatric aspects of SLE.
Goal of this Research Topic is to understand how IFN family members and other proinflammatory mediators are associated with specific lupus clinical phenotypes or disease endotypes.
In this article collection, we aim to include manuscripts that describe the role of interferons and other proinflammatory mediators in lupus including but not limited to: skin, vasculature, kidney, CNS. These studies may describe insights into IFN family members as well as the interplay and networks of established and more novel proinflammatory cytokines and their receptors.
Guest Editors declaration:
1. WIW is an employee of AstraZeneca and owns stock in AstraZeneca.
2. JMR is an inventor on use patents filed for “Diagnosis of skin conditions in veterinary and human patients”, and for targeting CXCR3 (0#15/851,651) and IL15 (# 62489191) for the treatment of vitiligo.