Anne M Stevens, MD, PhD

Anne M Stevens, MD, PhD

Specialties

  • Academic Title: Affiliate Clinical Professor
  • On Staff Since: July 2000
"Many years ago, I began caring for a child with severe lung disease due to scleroderma, an autoimmune condition in which inflammation of the skin and lungs leads to scarring. At the time, the five-year survival rate for scleroderma was only 50%. Although the patient missed a lot of school during treatment, she stayed healthy with her parents’ support. She even played varsity basketball in high school. Her father once worried that he’d never see her grow up. Now he thinks he might be able to walk her down the aisle someday. Patients like her motivate me to advance scientific understanding of scleroderma and other diseases and to hopefully discover new treatments through laboratory research."

  • Biography

    Board Certification(s)

    Pediatric Rheumatology

    Education

    Baylor College of Medicine, Houston, TX

    Residency

    Children's Hospital & Medical Center, Seattle, WA

    Fellowship

    University of Washington School of Medicine, Seattle, WA

    Clinical Interests

    Role of maternal microchimerism in pediatric systemic lupus erythematosus and scleroderma

    Research Description

    The Stevens Lab is focused on the role of maternal microchimerism and T lymphocyte regulation in children with systemic lupus erythematosus (SLE).

    There are two major projects:

    1) Maternal Microchimerism in Systemic Lupus.

    The role that maternal cells, passing into the fetus during pregnancy and persisting for years in the child, play in the pathogenesis of autoimmune diseases. The lab has demonstrated that maternal cells can differentiate into myocardial cells in the hearts of infants with neonatal lupus syndrome, where these foreign cells may act as targets for the child's immune system. Maternal cells in children can also become liver cells, kidney cells, and pancreatic islet cells.

    Current work aims to answer the question: do maternal cells, expressing foreign proteins, act to stimulate the child's immune system in these organs, leading to chronic inflammatory diseases like lupus? Or do maternal cells respond to tissue injury and aid in repair of tissue injured by inflammation due to another cause? To answer this question, the lab is studying the immune response to chimeric maternal cells in children with Systemic Lupus Erythematosus (SLE) and a mouse model investigating the role of maternal cells in renal injury.

    2) The Loss of the Negative Regulator PD-L1 on Dendritic Cells and Monocytes in Children with SLE.

    The loss of the negative regulator PD-L1 on dendritic cells and monocytes in children with SLE. This loss of a protein that inhibits T lymphocytes may lead to chronic inflammation in SLE. The Stevens Lab members are studying how PD-L1 is regulated, and exploring the use of PD-L1 as a biomarker for SLE disease activity or replacing PD-L1 as a treatment.

    Students currently training in the lab include: Brian Harrington, James Kuo.
    Post-Doctoral Fellow: Jing-Ni Ou, PhD

    Research Focus Area

    Autoimmune Diseases

  • Patient Testimonials

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  • Awards and Honors

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  • Publications

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  • Research Funding

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  • Clinical Trials and Research

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