Targeting B cells in the pre-phase of systemic autoimmunity globally interferes with autoimmune pathology

Systemic lupus erythematosus (SLE) is characterized by a loss of self-tolerance, systemic inflammation, and multi-organ damage. While a variety of therapeutic interventions are available, it has become clear that an early diagnosis and treatment may be key to achieve long lasting therapeutic responses and to limit irreversible organ damage. Loss of humoral tolerance including the appearance of self-reactive antibodies can be detected years before the actual onset of the clinical autoimmune disease, representing a potential early point of intervention. Notmuch is known, however, about how and to what extent this pre-phase of disease impacts the onset and development of subsequent autoimmunity. By targeting the B cell compartment in the pre-disease phase of a spontaneous mouse model of SLE we now show, that resetting the humoral immune system during the clinically unapparent phase of the disease globally alters immune homeostasis delaying the downstream development of systemic autoimmunity.

Automated summary

Systemic lupus erythematosus (SLE) is characterized by loss of self-tolerance, systemic inflammation, and multi-organ damage. Early diagnosis and treatment are crucial for achieving long-lasting therapeutic responses and limiting irreversible organ damage. Loss of humoral tolerance before clinical autoimmune disease onset provides a potential early intervention point.