Autoimmune diseases can be broadly divided into two types depending on the principal clinical and pathological disease features: those that damage many organs (systemic), and those where only a single organ or tissue is directly damaged by the autoimmune process (localized).

Systemic autoimmune diseases are often characterized by autoantibodies reactive with a wide variety of autoantigens including DNA, cell surface molecules, and intracellular matrix proteins. Although the causes of systemic autoimmunity remain unclear, several immunological mechanisms have been implicated, along with genetic and environmental factors.

This portfolio primarily supports basic and translational studies of systemic lupus erythematosus (SLE) and autoimmune myositis. Areas of focus include:

  • Animal models of disease.
  • Animal model-based genetic studies to discover and evaluate candidate susceptibility genes.
  • Involvement of the innate immune system on the initiation and propagation of autoimmune disease.
  • B and T cell development, differentiation, homeostasis, and tolerance.
  • Role of regulatory lymphoid cells.
  • Molecular mechanisms that incite or dampen inflammation.
  • Interactions between antigen presenting cells, such as dendritic cells and T cells.
  • Cross-talk between immune cells and fibroblasts.
  • Fc gamma receptors and immune complexes on disease etiology and pathology.
  • Studies of apoptosis and clearance of apoptotic bodies.
  • Mechanisms of end-organ damage, including the pathophysiology of disease-associated autoantibodies.
  • Basic research on treatments.

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Marie Mancini, Ph.D.

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6701 Democracy Boulevard
Building: Democracy 1, Suite 800
Bethesda MD 20892-4872

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Last Updated: October 2019