Department of Immunology

Jane Buckner, M.D.


Dr. Buckner graduated magna cum laude from Carleton College in 1983, and received her medical degree from The Johns Hopkins University School of Medicine in 1987. She received postdoctoral training at the Benaroya Research Institute at Virginia Mason. She joined the faculty of the Benaroya Research Institute in 1999, where she is now President, and Director of Translational Research.


Jane Buckner, M.D., President
Benaroya Research Institute
at Virginia Mason
1201 Ninth Avenue Seattle, WA 98101
Ph: 206.287.1033 Fax: 206.223.7638

Assistant Contact:
Wendy Kliment
Executive Assistant to the President
Ph: 206.342.6595


Tolerance & Autoimmunity


Elizabeth Dam
Tania Habib
Christian Hundhausen
Mackenzie Kinsman
Alison Maier
Tuan Nguyen
Cliff Rims
Charles Smarr
Megan Tatum
Hannes Uchtenhagen



Buckner Lab





Dr. Buckner’s research focuses on identifying the underlying mechanisms by which the adaptive immune response to self-antigens becomes pathogenic in the setting of human autoimmune disease. To this end, Dr. Buckner’s group studies how both regulatory and effector mechanisms are altered in autoimmunity.

The lab works on three areas of autoimmunity:

  1. Genetic variants associated with autoimmune disease. Dr. Buckner’s group has a long-standing interest in determining the functional impact of genetic variants associated with type 1 diabetes and lupus including PTPN22, IL2RA, PTPN2, BANK1, IFIH1 and TYK2. Their work has shown that the PTPN22 risk variant alters B cell signaling and B cell development, and their studies of both the IL2RA and the PTPN2 risk variants associated with T1D have demonstrated an association with reduced responsiveness to IL-2 signaling in regulatory T cells in type 1 diabetes and multiple sclerosis. Ongoing phenotype-genotype studies are determining the functional impact of additional risk variants, alone and in combination, on specific programs implicated in autoimmune disease. Their approach in collaboration with Dr. David Rawlings, Seattle Children’s Research Institute, integrates studies of primary human cells from healthy controls and individuals with autoimmune disease, novel mouse models, and innovative gene editing technologies.
  2. Cytokine signaling pathways in the development and progression of autoimmune disease. The Buckner group’s work on IL-2 signaling highlights the importance of this pathway in the maintenance of FOXP3 expression in regulatory T cells in type 1 diabetes. Furthermore, recent work from the Buckner lab has shown that the T cell response to IL-6 signaling is enhanced in type 1 diabetes and relapsing-remitting multiple sclerosis. Ongoing studies are investigating how alterations in response to cytokine signalinginfluence the expansion and persistence of pathogenic autoreactive effector T cells. These studies examine the response to cytokine signaling in the context of clinical, genetic and immunologic heterogeneity of human subjects, which is critical for the development of precision medicine for the prevention and treatment of autoimmune disease.
  3. Antigen-specific T cells in rheumatoid arthritis. These studies are characterizing antigen-specific T cells in rheumatoid arthritis using tools that include multiplex tetramer approaches. The long-term goal of these studies is to understand the specificity of the pathogenic response in rheumatoid arthritis, and to determine how the frequency and phenotype of antigen-specific T cells is altered with respect to disease activity and response to therapy. Recent work from the Buckner lab has shown that citrulline-specific Th1 cells are increased in rheumatoid arthritis and that the frequency of these cells is influenced by disease duration and therapy. The Buckner group is also assessing antigen-specific T cell responses with respect to T cell repertoire and transcriptional profile in both individuals with rheumatoid arthritis and in individuals at high risk for rheumatoid arthritis.


  1. Cerosaletti K, Schneider A, Schwedhelm K, Frank I, Tatum M, Wei S, Whalen E, Greenbaum C, Kita M, Buckner J, Long SA. Multiple autoimmune-associated variants confer decreased IL-2R signaling in CD4+ CD25(hi) T cells of type 1 diabetic and multiple sclerosis patients. PLoS One. 2013 Dec 23;8(12):e83811.
  2. Habib T, Funk A, Rieck M, Brahmandam A, Dai X, Panigrahi AK, Luning Prak ET, Meyer-Bahlburg A, Sanda S, Greenbaum C, Rawlings DJ, Buckner JH. Altered B cell homeostasis is associated with type I diabetes and carriers of the PTPN22 allelic variant. J Immunol. 2012 Jan 1;188(1):487-96.
  3. Dai X, James RG, Habib T, Singh S, Jackson S, Khim S, Moon RT, Liggitt D, Wolf-Yadlin A, Buckner JH, Rawlings DJ. A disease-associated PTPN22 variant promotes systemic autoimmunity in murine models. J Clin Invest. 2013 May;123(5):2024-36.
  4. Long SA, Cerosaletti K, Bollyky PL, Tatum M, Shilling H, Zhang S, Zhang ZY, Pihoker C, Sanda S, Greenbaum C, Buckner JH. Defects in IL-2R signaling contribute to diminished maintenance of FOXP3 expression in CD4(+)CD25(+) regulatory T-cells of type 1 diabetic subjects. Diabetes. 2010 Feb;59(2):407-15.
  5. Hundhausen C, Roth A, Whalen E, Chen J, Schneider A, Long SA, Wei S, Rawlings R, Kinsman M, Evanko SP, Wight TN, Greenbaum CJ, Cerosaletti K, Buckner JH. Enhanced T cell responses to IL-6 in type 1 diabetes are associated with early clinical disease and increased IL-6 receptor expression. Sci Transl Med. 2016 Sep 14;8(356):356ra119.
  6. Schneider A, Long SA, Cerosaletti K, Ni CT, Samuels P, Kita M, Buckner JH. In active relapsing-remitting multiple sclerosis, effector T cell resistance to adaptive T(regs) involves IL-6-mediated signaling. Sci Transl Med. 2013 Jan 30;5(170):170ra15.
  7. James EA, Rieck M, Pieper J, Gebe JA, Yue BB, Tatum M, Peda M, Sandin C, Klareskog L, Malmström V, Buckner JH. Citrulline-specific Th1 cells are increased in rheumatoid arthritis and their frequency is influenced by disease duration and therapy. Arthritis Rheumatol. 2014 Jul;66(7):1712-22.