Principal Investigator

Mariana J. Kaplan, M.D.

Prior to joining the NIAMS, Dr. Mariana Kaplan was on faculty at the University of Michigan. As chief of the Systemic Autoimmunity Branch, she works to identify mechanisms of organ damage and premature vascular disease in systemic autoimmunity.

Systemic autoimmune diseases are a group of disorders characterized by a failure in self-tolerance to a wide variety of autoantigens, and include conditions like systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and anti-neutrophil cytoplasmic antibody associated-vasculitis (AAV). These disorders are very heterogeneous, but they have some commonalities. For instance, all appear to manifest after multi-step processes where genetic and environmental factors play key roles in predisposing individuals to a higher risk of establishing abnormal innate and adaptive immune responses. Subclinical immune dysregulation eventually leads to a pre-clinical phase of variable duration (sometimes decades), during which autoantibodies to specific antigens are synthesized. It is believed that exposure to a variety of additional environmental hits may be required to trigger the acute clinical manifestations that are characteristic of these specific conditions.

As treatments to suppress aberrant immune responses have improved and patients are able to survive for longer periods of time, the prevalence of end-stage complications, such as development of accelerated atherosclerosis not explained by traditional cardiovascular risk factors, has increased. We need to identify the susceptibility triggers that lead to a break in tolerance, as well as enhance our understanding of the innate and adaptive immune pathways crucial to initiate and perpetuate these autoimmune responses. In addition, we need to better identify the mechanisms that lead to specific clinical phenotypes and promotion of end-organ damage.

The broad and long-term objectives of the Systemic Autoimmunity Branch are to further the understanding of the clinical spectrum and pathophysiology of systemic autoimmune diseases, and to translate this knowledge into better therapies that improve outcomes for patients with these conditions. A major goal of the Systemic Autoimmunity Branch is to combine natural history or treatment studies with basic investigations into the etiology and/or pathophysiology of rheumatic diseases, with an emphasis on SLE, AAV, RA and other systemic autoimmune diseases affecting adults. Additionally, the branch works to train the next generation of scientists and physician scientists focused on the understanding of the pathogenesis and advancement in the treatments of patient afflicted by systemic autoimmune diseases.

Current areas of interest of the branch include:

  • The role of neutrophils and neutrophil extracellular traps (NETs) in induction of loss of immunologic tolerance and acceleration of organ and vascular damage.
  • How type I Interferons (IFNs) contribute to the development of premature atherogenesis and vasculopathy in SLE and other connective tissue diseases.
  • Identification of novel biomarkers and therapeutic targets to mitigate CV damage and induce immunomodulation in SLE and other systemic rheumatic diseases.


Senior Investigator and Chief, Systemic Autoimmunity Branch
Associate Director NIAMS Fellowship Program, Systemic Autoimmunity Branch
Predoctoral Trainee, Systemic Autoimmunity Branch
Postbaccalaureate Fellow, Systemic Autoimmunity Branch
Assistant Research Physician, Lupus Clinical Trials Unit
Postdoctoral Fellow, Systemic Autoimmunity Branch
Clinical Research Coordinator, Systemic Autoimmunity Branch
Henry Metzger Scholar in Translational Medicine, Systemic Autoimmunity Branch
Postbaccalaureate Fellow, Systemic Autoimmunity Branch
Postbaccalaureate Fellow, Systemic Autoimmunity Branch
Visiting Scientist, Systemic Autoimmunity Branch

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Latest News

Research Brief | February 23, 2016

Mitochondria Found to Play Instrumental Role in NET Formation and Autoimmune Disease

Neutrophil extracellular traps (NETs) are web-like structures that immune cells called neutrophils use to ensnare and kill microbes such as bacteria or fungi. Some evidence suggests that NETs, which contain an individual’s own cellular proteins and DNA, can trigger an immune reaction to these "self" components and promote autoimmunity.
Announcement | December 8, 2015

NIAMS’ Kaplan Honored for Lupus Research

Mariana Kaplan, M.D., Chief of the Systemic Autoimmunity Branch in the NIAMS Intramural Research Program (IRP), recei

Last Updated: May 2020