Reflections on chromatin structures, corresponding autoantibodies - And conflicting dogmas impacting pathogenesis of lupus nephritis.

This study concentrates on problems related to the inadequate integration of the causality principle, and on central historical data that are disregarded in SLE research. Three research areas will be critically discussed: i. Role of SLE-associated causality principle and causality cascade; ii. Definition and clinical impact of anti-B DNA structure-specific and anti-chromatin-specific antibodies; iii. Incompatible pathogenic models that account for lupus nephritis, and their individual theoretical impacts on causal therapy development. A main motivation is to revitalize ignored but highly important historical milestone discoveries, and documentation of concrete problems that have not been studied seriously like nosology connected to rationalizing SLE as a disease entity. This study covers description of anti-DNA antibody structures and anti-chromatin antibodies; their origins, and their impact on operational molecular and cellular processes accounting for lupus nephritis. The reflections around autoimmune diagnostics and pathophysiology provide information connected to "SLE as an enigmatic prototype autoimmune syndrome". We need to implement causality as a central element to promote rational hypotheses that may make SLE logic and intellectually understandable. This is critical if the research aim is to develop causal therapies. The manuscript is analytical in nature and provides solutions to central problems that may resolve the causality cascade, a systemic element of causation that define SLE as a rational and delimitated syndrome. We have to bring to the discussion forum processes connecting DNA/chromatin structures with tolerance and immunity, inflammation, pathogenesis of lupus nephritis - and to replace classification criteria with causality-related diagnostic criteria.