TNF and systemic lupus erythematosus: However, recent data increasingly describe strong associations between DIL and newer agents, such as TNF inhibitors.4 By inhibiting Th1 response, anti-TNFα agents could be assumed to trigger Th2 autoimmune reactivity, including SLE.5 Pathogenic hypotheses for the ATIL syndrome include a reduced CD44 expression influencing the clearance of apoptotic neutrophils and nuclear debris by phagocytes, thereby leading to autoantibody production against nuclear antigens and DNA.