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Arthritis and Immunology Research Program

Dr. Kovats In The News

OMRF scientists discover clue to link between estrogen and lupus

New OMRF finding could help improve vaccines

Susan Kovats, Ph.D. Assistant Member, Arthritis and Immunology Research Program

Research Interests
Autoimmune diseases preferentially afflict women, and female-male sex influences immune responses, suggesting that estrogens regulate inflammation and immunity. Indeed, immune cells and their progenitors express estrogen receptors (ER). We study the role of ER in the development and function of cells of the innate immune system, termed dendritic cells. These cells are important for initiation of both innate and adaptive immunity. Inflammation and autoimmunity are associated with de novo dendritic cell development from inflammatory monocytes or bone marrow precursors. Our previous studies determined that ER signaling is an important positive regulator of this pro-inflammatory developmental pathway. Our current studies continue to focus on the role of ER signaling in dendritic cell development, as well as function, in healthy mice and in murine models of systemic autoimmunity and atherosclerosis.

ER act as ligand-dependent transcription factors that participate in chromatin-modifying complexes and thus regulate gene expression programs. Recently, we identified the transcription factor interferon regulatory factor 4 (Irf4) as an estradiol-regulated gene during the GM-CSF-induced differentiation of dendritic cells. Our data show that estradiol/ER signaling promotes dendritic cell differentiation by increasing and sustaining expression of IRF4 in myeloid progenitors. Ongoing experiments are defining molecular mechanisms by which ER signaling regulates the Irf4 gene.

To study how ER signaling regulates dendritic cell development in vivo, we are generating mixed ER⁺/ER^-/- bone marrow chimeric mice. These experiments have shown that ER expression differentially regulates dendritic cell and monocyte/macrophage development during inflammation and homeostasis. To study how ER signaling regulates post-developmental immune function, we are developing novel murine models in which ER deficiency is restricted to either DC or B lymphocytes.

Our long-term goals are to define the molecular mechanisms by which ER signaling regulates dendritic cell differentiation from bone marrow progenitors, and to understand how ER signaling modulates dendritic cell development and functional responses in vivo. We are applying the information gained from such studies to murine models of autoimmunity and atherosclerosis.

Joined OMRF Scientific Staff in 2005.

Mailing Address
Arthritis and Immunology Research Program, MS 24
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, Oklahoma 73104

Contact Information
Phone: (405) 271-8583
Fax: (405) 271-7063
E-mail: Susan-Kovats@omrf.org