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Related Experiment Videos

Autoimmunity and bone.

Edward M Schwarz1, R John Looney, M Hicham Drissi

  • 1Department of Orthopaedics, University of Rochester Medical Center, 601 Elmwood Avenue, Box 665, Rochester, NY 14642, USA. Edward_Schwarz@URMC.Rochester.Edu

Annals of the New York Academy of Sciences
|July 13, 2006
PubMed
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Systemic tumor necrosis factor (TNF) drives osteoclast formation in psoriatic arthritis (PsA), while interferon-alpha (IFN-alpha) promotes dendritic cell differentiation in lupus. This axis dictates bone erosion in autoimmune diseases.

Area of Science:

  • Immunology
  • Rheumatology
  • Bone Biology

Background:

  • Autoimmune inflammatory arthritis, including rheumatoid arthritis (RA) and psoriatic arthritis (PsA), causes debilitating joint erosions.
  • Osteoclast precursors (OCP) from bone marrow migrate and differentiate into bone-resorbing osteoclasts, a process influenced by systemic factors.
  • Systemic lupus erythematosus (SLE) patients exhibit resistance to bone resorption, unlike RA and PsA patients.

Purpose of the Study:

  • To test the hypothesis that systemic tumor necrosis factor (TNF) induces osteoclastic differentiation of peripheral blood mononuclear cells (PBMC) in psoriatic arthritis (PsA) patients, correlating with erosive disease.
  • To investigate if the innate immune TNF/IFN axis dictates the erosive phenotype in autoimmune diseases.
  • To explore the impact of systemic factors on myelopoiesis and bone homeostasis.

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Main Methods:

  • Utilized a tumor necrosis factor (TNF) transgenic mouse model of erosive arthritis and analyzed anti-TNF clinical trials in PsA patients.
  • Investigated the role of systemic interferon-alpha (IFN-alpha) in diverting myeloid precursors away from osteoclast lineage towards dendritic cell (DC) differentiation in SLE.
  • Injected wild-type and TNF-Tg mice with poly I:C to induce systemic IFN responses and analyzed changes in circulating CD11b+/CD11c+ precursor dendritic cells (pDC) and CD11b+/CD11c- OCP.

Main Results:

  • Systemic TNF was shown to induce the migration of CD11b+ osteoclast precursors (OCP) from bone marrow into peripheral blood, facilitating joint entry and osteoclast differentiation.
  • Systemic IFN-alpha in SLE patients was hypothesized to divert myeloid precursors to dendritic cells (DC), explaining resistance to bone resorption.
  • Poly I:C injection in mice demonstrated dominant effects on increasing pDC and reducing OCP, highlighting the impact of systemic IFN on myelopoiesis.

Conclusions:

  • The systemic TNF/IFN axis in autoimmune diseases critically influences the balance between osteoclast and dendritic cell differentiation.
  • This axis dictates the distinct erosive or non-erosive phenotypes observed in different autoimmune conditions.
  • Systemic factors profoundly impact myelopoiesis and bone homeostasis in autoimmunity.