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Assistant Professor, Division of Nephrology and Hypertension

Specialty Areas

Cell biology; Immunology; Regulatory B cells; B cell development; Autoantibodies; Glomerular disease; Autoimmunity

Education and Experience

BA: University of North Carolina, 1980; PhD: Duke University, 1991; Research Associate: National Research Council, 1991-4; Training Award Fellow: National Institute of Environmental Health Sciences, 1994-7; Postdoctoral Research Associate: University of North Carolina, 1997-2000; Assistant Professor: University of North Carolina, 2000-Present.

Research Interests

Donna Bunch’s research focuses on dissecting the role of B cells and the autoantibodies they produce in autoimmune diseases affecting the kidney. She investigates the immune dysregulation that triggers production of pathogenic autoantibodies and how these autoantibodies interact with immune cells (B cells, neutrophils, monocytes and dendritic cells) to generate microparticles or cause the release of cytokines and other cellular factors that regulate the network of cells comprising the immune system. She is particularly interested in elucidating the mechanisms by which regulatory B cells help maintain immunological balance and promote disease remission.

Dr. Bunch’s goal is to translate what we know about disease pathogenesis into better clinical tools for predicting relapse or other disease complications such as thrombosis and better therapies for management of diseases affecting the kidney.

Selected Bibliography

  1. Aybar LT, McGregor JG, Hogan SL, Hu Y, Mendoza CE, Brant EJ, Poulton CJ, Henderson CD, Falk RJ,Bunch DO. Reduced CD5+ CD24hi CD38hi and interleukin-10+ regulatory B cells in active anti-neutrophil cytoplasmic autoantibody-associated vasculitis permit increased circulating autoantibodies. Clin Exp Immunol. 2015 May;180(2):178-88. PubMed PMID: 25376552; PubMed Central PMCID: PMC4408152.
  2. Reynolds J, Preston GA, Pressler BM, Hewins P, Brown M, Roth A, Alderman E, Bunch D, Jennette JC, Cook HT, Falk RJ, Pusey CD. Autoimmunity to the alpha 3 chain of type IV collagen in glomerulonephritis is triggered by ‘autoantigen complementarity’. J Autoimmun. 2015 May;59:8-18. PubMed PMID: 25841937.
  3. Bunch DO, Mendoza CE, Aybar LT, Kotzen ES, Colby KR, Hu Y, Hogan SL, Poulton CJ, Schmitz JL, Falk RJ, Nachman PH, Pendergraft WF, McGregor JG. Gleaning relapse risk from B cell phenotype: decreased CD5+ B cells portend a shorter time to relapse after B cell depletion in patients with ANCA-associated vasculitis. Ann Rheum Dis. 2015 Apr 30; PubMed PMID: 25934841.
  4. McGregor JG, Hogan SL, Kotzen ES, Poulton CJ, Hu Y, Negrete-Lopez R, Kidd JM, Katsanos SL, Bunch DO, Nachman PH, Falk RJ. Rituximab as an immunosuppressant in antineutrophil cytoplasmic antibody-associated vasculitis. Nephrology, Dialysis, and Transplantation. 2015; 30 Suppl 1:i123-31. PubMed PMID: 25805743; PMCID: PMC4447867.
  5. Free ME, Bunch DO, McGregor J, Jones BE, Berg EA, Hogan SL, Hu Y, Preston GA, Jennette JC, Falk RJ, Su MA. Patients with Antineutrophil Cytoplasmic Antibody-associated Vasculitis Have Defective Treg Function Exacerbated by the Presence of a Suppression-Resistant Effector Cell Population. 2013, Arthritis and Rheumatism, 65:1922-33. NIHMSID: NIHMS475823; PubMed PMID: 23553415; PMCID: PMC3717615.
  6. Bunch DO, McGregor JAG, Khandoobhai NB, Aybar LT, Burkart ME, Hu Y, Hogan SL, CE Jennette, Berg EA, Falk RJ, Nachman PH. Decreased CD5+ B Cells in Active Anti-neutrophil Cytoplasmic Autoantibody (ANCA) Vasculitis and Relapse after Rituximab. 2013, CJASN, 8:382-91. PubMed PMID: 23293123; PubMed Central PMCID: PMC3586963.
  7. Roth AJ, Brown MC, Smith RN, Badhwar AK, Parente O, Chung HC, Bunch DO, McGregor JG, Hogan SL, Hu Y, Yang JJ, Berg EA, John Niles J, Jennette JC, Preston GA and Falk RJ. Anti-LAMP-2 antibodies are not prevalent in patients with Anti-neutrophil Cytoplasmic Autoantibody Glomerulonephritis. 2012, Journal of the American Society of Nephrology, 23:545-55. PubMed PMID: 22021709; PubMed Central PMCID: PMC3294309.
  8. Cao Y, Schmitz JL, Yang J, Hogan SL, Bunch D, Hu Y, Jennette CE, Berg EA, Arnett FC Jr, Jennette JC, Falk RJ, Preston GA. DRB1*15 Allele Is a Risk Factor for PR3-ANCA Disease in African Americans. 2011, Journal of the American Society of Nephrology, 22:1161-7. PubMed PMID: 21617122; PMCID: PMC3103736.
  9. Bunch DO, Silver JS, Majure MC, Sullivan P, Alcorta DA, Chin H, Hogan SL, Lindstrom YI, Clarke SH, Falk RJ, and Nachman PH. Maintenance of Tolerance by Regulation of Anti-Myeloperoxidase B Cells. 2008, Journal of the American Society of Nephrology, 19:1763-73.
  10. Culton D, Nichols MG, Bunch DO, Zhen QL, Kepler TB, Dooley MA, Mohan C, Nachman PH, and Clarke SH. Similar CD19 Dysregulation in Two Autoantibody-associated Autoimmune Diseases Suggests a Shared Mechanism of B Cell Tolerance Loss. 2007, Journal of Clinical Immunology, 27:53-68.
  11. Erdbrügger U., Hellmark T, Bunch DO, Alcorta DA, Jennette JC, Falk RJ, Nachman PH. Mapping Of Myeloperoxidase (MPO) Epitopes Recognized By MPO-ANCA Using Human-Mouse MPO Chimers. 2006, Kidney International, 69:1799-1805.

View list of publications on PubMed.