Mary Helen Foster, MD

Professor of Medicine
Member of the Duke Cancer Institute
Campus mail Duke Box 103015, Durham, NC 27710
Phone (919) 684-9788
Email address foste027@duke.edu

Research in the Foster Lab focuses on autoimmune glomerulonephritis, a major cause of acute and chronic kidney disease worldwide.

Our experiments explore the origins and regulation of the pathogenic immune  responses that underlie glomerulonephritis, and are designed to: identify tolerance mechanisms that regulate nephritogenic lymphocytes, with an emphasis on B cells and autoantibodies; determine the molecular basis of tolerance; identify defects in immune regulation and the contributions of genetic autoimmune predisposition; and identify environmental disease triggers. These experiments use novel models relevant to immune nephritis in both kidney-restricted and systemic autoimmunity (Goodpasture syndrome and systemic lupus erythematosus, respectively), that are amenable to mechanistic dissection using basic immunological, molecular biological, and proteomics approaches. An ultimate goal is to advance novel diagnostic and therapeutic approaches to improve the lives of patients.

Education and Training

  • Fellow in Nephrology, Medicine, Tufts University, 1985 - 1989
  • Medical Resident, Medicine, University of Virginia, 1982 - 1985
  • M.D., University of North Carolina - Chapel Hill, 1982

Publications

Foster, Mary H., Jeffrey R. Ord, Emma J. Zhao, Anastasiya Birukova, Lanette Fee, Francesca M. Korte, Yohannes G. Asfaw, et al. “Silica Exposure Differentially Modulates Autoimmunity in Lupus Strains and Autoantibody Transgenic Mice.” Front Immunol 10 (2019): 2336. https://doi.org/10.3389/fimmu.2019.02336.

PMID
31632407
Full Text

Ord, Jeffrey R., Amy G. Clark, and Mary H. Foster. “Shared Genetic Origins Among Anti-Proteinase 3 and Anti-Glomerular Basement Membrane Double-Positive Human Autoantibodies.” In Arthritis & Rheumatology, Vol. 70. WILEY, 2018.

Scholars@Duke

Clark, Amy G., Elizabeth S. Buckley, and Mary H. Foster. “Altered toll-like receptor responsiveness underlies a dominant heritable defect in B cell tolerance in autoimmune New Zealand Black mice.” Eur J Immunol 48, no. 3 (March 2018): 492–97. https://doi.org/10.1002/eji.201747287.

PMID
29251774
Full Text

Clark, Amy G., Inge M. Worni-Schudel, Francesca M. Korte, and Mary H. Foster. “A murine Ig light chain transgene reveals IGKV3 gene contributions to anti-collagen types IV and II specificities.” Mol Immunol 91 (November 2017): 49–56. https://doi.org/10.1016/j.molimm.2017.08.015.

PMID
28886586
Full Text

Foster, Mary H. “Optimizing the translational value of animal models of glomerulonephritis: insights from recent murine prototypes.” Am J Physiol Renal Physiol 311, no. 3 (September 1, 2016): F487–95. https://doi.org/10.1152/ajprenal.00275.2016.

PMID
27335377
Full Text

Foster, Mary H., Elizabeth S. Buckley, Benny J. Chen, Kwan-Ki Hwang, and Amy G. Clark. “Uncommon structural motifs dominate the antigen binding site in human autoantibodies reactive with basement membrane collagen.” Mol Immunol 76 (August 2016): 123–33. https://doi.org/10.1016/j.molimm.2016.07.004.

PMID
27450516
Full Text

Worni-Schudel, Inge M., Amy G. Clark, Tiffany Chien, Kwan-Ki Hwang, Benny J. Chen, and Mary H. Foster. “Recovery of a human natural antibody against the noncollagenous-1 domain of type IV collagen using humanized models.” J Transl Med 13 (June 6, 2015): 185. https://doi.org/10.1186/s12967-015-0539-4.

PMID
26048777
Full Text

Pages