Macrophages and neutrophils in SLE—An online molecular catalog

Autoantibodies specific to D4GDI modulate Rho GTPase mediated cytoskeleton remodeling and induce autophagy in T lymphocytes

“…However, it is likely that the complex interaction between genetic, environmental (e.g., infectious agents, UV light, drugs), and hormonal factors promotes the immune dysfunction underlying the pathogenesis of the disease. SLE is characterized by autoantibody production by deregulated B cells, target organ infiltration by inflammatory T cells and aberrant immune cell activation due to abnormal antigenpresenting cell function [2,3]. Among the cells that participate in the initiation, progression, and perpetration of the disease, T lymphocytes play a key role in all stages [4].…”

Heightened cleavage of Axl receptor tyrosine kinase by ADAM metalloproteases may contribute to disease pathogenesis in SLE

“…Adaptive immune dysfunction produces autoantibodies leading to immune complex formation and deposition in the skin, joints, and kidneys. Innate immunity plays an important role in determining disease severity and progression [2]. Factors and pathways that modulate innate immunity impact the course of disease, particularly in end organ systems where most major, life-threatening disease manifestations occur.…”

Gene profiling reveals specific molecular pathways in the pathogenesis of atherosclerosis and cardiovascular disease in antiphospholipid syndrome, systemic lupus erythematosus and antiphospholipid syndrome with lupus

“…In addition to modulate lipid metabolism, monocytes secrete inflammatory cytokines, chemokines and reactive oxygen species that drive the pathogenesis. They also produce TF and proteases that contribute to thrombosis and atherosclerotic plaque rupture 19 20. Characterising the monocytes molecular signature may provide an alternative and effective way to identify heterogeneous autoimmune patient's subpopulations for targeted therapies.…”