About this Research Topic
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.
Keywords: Type I interferons, IFNs, IFNa, IFNk, IL-21, IL-10, IL-2, IL-17, IL-23, CCL2, CCL-3-5, CXCL-10
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.