MU Logo Department of Internal Medicine at MUMu Health Care

Faculty Profiles

Helen Mullen, PhD

Professor of Medicine

Dr. Mullen's research is supported by the National Institutes of Health and the Department of Veterans Affairs. She has authored over 85 research publications in peer-reviewed journals. She has served on NIH study sections and is currently serving as a member of the VA Medical Research Advisory Group.

Dr. Mullen's current research is directed towards understanding the mechanisms involved in induction and regulation of autoimmune disease. For these studies, two different murine models of autoimmune thyroiditis, an experimentally induced (EAT) model and a spontaneous model of autoimmune thyroiditis (SAT) are used. In the EAT model, EAT is induced in recipients of in vitro-activated T cells from mouse thyroglobulin (MTg)-sensitized donors. Donor cells activated with Mtg and IL-12 induced a severe form of EAT with granulomatous histopathology (G-EAT) in the recipient thyroids. (see Figure). After reaching maximal severity 21 days after cell transfer, these G-EAT lesions either resolve (heal) or progress to end-stage fibrosis by day 35-40. The major focus of the current research in the laboratory is to define the underlying mechanisms that lead to these two distinct outcomes of the autoimmune inflammatory response, with the long-term goal being to devise means by which to promote resolution and prevent or reverse fibrosis. In the SAT model, NOD.H-2h4 mice spontaneously develop thyroid lesions and anti-MTg autoantibodies. The major focus of these studies is to understand the cellular mechanisms involved in this spontaneous reactivity to self, and to use this information to devise rational therapeutic strategies for prevention and treatment of autoimmune disease.

Photo of Dr. Mullen

Graduate School

PhD from Purdue University
West Lafayette, IN

Research Associate:

University of Missouri
Columbia, MO


Organizations:

  • Member- American Association of Immunologists
  • Ad Hoc Reviewer- National Science Foundation, VA Merit Review, Journal of Immunology
Selected Publications:
  1. Fang, Y., Wei, Y., DeMarco, V., Chen, K., Sharp, G., and H. Braley-Mullen. Murine FLIP transgene expressed on thyroid epithelial cells promotes resolution of granulomatous experimental autoimmune thyroiditis . Am. J. Pathol. (in press).
  2. Chen, K., Wei, Y., Sharp, G., and H. Braley-Mullen. Decreasing TNFα results in less fibrosis and earlier resolution of granulomatous experimental autoimmune thyroiditis. J. Leuk. Biol. (in press).
  3. Yu, S., Maiti, P., Dyson, M., Jain, R., and H. Braley-Mullen. CD4+CD25+ T regulatory cells inhibit development of spontaneous autoimmune thyroiditis in B cell-deficient NOD.H-2h4 mice. J. Exp. Med. 203:349-358, 2006
  4. Yu, S., Sharp, G. C., and H. Braley-Mullen. Thyrocytes responding to IFN-γ are essential for development of lymphocytic spontaneous autoimmune thyroiditis and for inhibition of thyrocyte hyperplasia. J. Immunol. 176: 1259-1265, 2006.
  5. Yu, S., Sharp, G. C., and H. Braley-Mullen. Thyroid epithelial cell hyperplasia in IFN-γ deficient NOD.H-2h4 mice. Clin. Immunol. 118: 92-100, 2006.
  6. Chen, K., Wei, Y., Sharp, G. C., and H. Braley-Mullen. Balance of proliferation and cell death between thyrocytes and myofibroblasts regulates thyroid fibrosis in granulomatous experimental autoimmune thyroiditis (G-EAT). J. Leuk. Biol., 177: 166-172, 2005.
  7. Wei, Y., Chen, K., Sharp, G. C., and H. Braley-Mullen. Expression of FLIP and FasL by inflammatory cells vs. thyrocytes correlates with chronic inflammation or resolution of autoimmune thyroiditis in mice. Clin. Immunol. 108: 221-233, 2003.
  8. Chen, K., Wei, Y., Sharp, G.C., and H. Braley-Mullen.  Mechanisms of spontaneous resolution vs. fibrosis in granulomatous experimental autoimmune thyroiditis (G-EAT).  J. Immunol. 171: 6236-6243, 2003.
  9. Wei, Y., Chen, K., Sharp, G. C., and H. Braley-Mullen. Expression of FLIP and FasL by inflammatory cells vs. thyrocytes can be predictive of chronic inflammation or resolution of autoimmune thyroiditis in mice.  Clinical Immunol.  108: 221-233, 2003.
  10. Chen, K., Wei, Y., Sharp, G. C., and H. Braley-Mullen. Inhibition of thyroid fibrosis in a murine model of granulomatous experimental autoimmune thyroiditis by anti-TGFb or Lisinopril treatment.  J. Immunol., 169: 6530-6538, 2002.
  11. Yu, S., Sharp, G. C., and H. Braley-Mullen.  Dual roles for IFNg, but not for IL-4 in spontaneous autoimmune thyroiditis in NOD.H-2h4 mice.  J. Immunol., 169: 3999-4007, 2002.
  12. Wei, Y., Chen, K., Sharp, G.C., Yagita, H., and H. Braley-Mullen. Expression and regulation of Fas and FasL on thyrocytes and infiltrating cells during induction and resolution of granulomatous experimental autoimmune thyroiditis. J. Immunol. 167: 6678-6686, 2001.
  13. Yu, S., Medling, B.Yagita, H., and H. Braley-Mullen. Characteristics of inflammatory cells in spontaneous autoimmune thyroiditis of NOD.H-2h4 mice. J. Autoimmunity 16: 37-46, 2001.
  14. Chen, K., Wei, Y. Sharp, G., and H. Braley-Mullen. 2001. Induction of experimental autoimmune thyroiditis in IL-12-/-mice. J. Immunol. 167:1720-1727.
  15. Yu, S., Medling, B., Yagita, B., and H. Braley-Mullen. 2001. Characteristics of inflammatory cells in spontaneous autoimmune thyroiditis of NOD.H-2h4 mice. J. Autoimmunity. 16:37-46.
  16. Wei, Y., Chen, K., Sharp, G., Yagita, H. and H. Braley-Mullen. 2001. Expression and regulation of Fas and FasL on thyrocytes and infiltrating cells during induction and resolution of granulomatous experimental autoimmune thyroiditis. J. Immunol. 167:6678-6686.
  17. Braley-Mullen, H., and S. Yu. 2000. Early requirement for B cells for development of spontaneous autoimmune thyroiditis in NOD.H-2h4 mice. J. Immunol. 165:7262-7269.
  18. Chen, K., Sharp, G., Wei, Y., and H. Braley-Mullen. 2000. Characterization of thyroid fibrosis in a murine model of granulomatous experimental autoimmune thyroiditis. J. Leuk. Biol. 68:828-835.
  19. Tang G, Sharp GC, Chen K, Braley-Mullen H. 1998. The kinetics of cytokine gene expression in the thyroids of mice developing granulomatous experimental autoimmune thyroiditis. J Autoimmun 11:581-589.
  20. Tang H, Sharp GC, Peterson KE, Braley-Mullen H. 1998. IFN-gamma-deficient mice develop severe granulomatous experimental autoimmune thyroiditis with eosinophil infiltration in thyroids. J Immunol 160:5105-5112
  21. Peterson K, Sharp GC, Tang H, Braley-Mullen H. 1999. B7.2 has opposing roles during the activation versus effector stages of experimental autoimmune thyroiditis. J Immunol 162:1859-1867.
  22. Braley-Mullen H, Sharp GC, Medling B, Tang H. 1999. Spontaneous autoimmune thyroiditis in NoD.H.2h4 mice. J Autoimmun 12:157-165.
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