The Molecular and Cellular Basis for Lupus

Dear Colleagues,

Systemic lupus erythematosus (SLE) is an autoimmune condition with a complicated pathophysiology that is not completely understood. While many molecular pathways and cellular alterations have been postulated and published in the literature, a number of clinical trials addressing these potentially pathological mechanisms have disappointingly failed to reach their respective primary endpoints, leading to the current paucity of targeted therapeutic agents that are capable of decelerating and even terminating the disease process and damage.

Nevertheless, some early and promising signals such as the success of the manipulation of the BAFF/ARPIL system, antagonization of IL-12/23 and the use of IL-2 in the management of SLE are currently in the pipeline for further evaluation for the clinical management of SLE. Obviously, these potential successes will not materialize if the basic molecular and cellular mechanisms of these new targets that are involved in the pathophysiology of SLE are not fully explored, vigorously tested and meticulously monitored.

This Special Issue of Cells aims to summarize the cutting-edge knowledge on the molecular and cellular basis of the pathogenesis and pathophysiology of SLE, in the hope of expanding the treatment armamentarium and ultimately, personalized treatment for patients with SLE.

We are looking forward to your significant contributions.

Dr. Anselm Mak
Guest Editor

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