Shaun W. Jackson, MB ChB, PhD

Nephrology, Rheumatology

On staff since July 2012

Academic Title: Associate Professor

Research Center: Center for Immunity and Immunotherapies

  • Shaun Jackson, MD, PhD, is an attending physician in Pediatric Nephrology and Pediatric Rheumatology at Seattle Children's Hospital and an Associate Professor of Pediatrics of Pediatrics at the University of Washington School of Medicine. After receiving his medical degree from the University of Cape Town in South Africa, he undertook post-doctoral studies in vascular biology at Harvard Medical School and completed pediatric residency training at Boston Children's Hospital. He completed dual pediatric nephrology and rheumatology fellowship training at Seattle Children's Hospital / University of Washington.

    During his fellowship, Dr Jackson worked in the B cell immunology laboratory of Dr. David Rawlings at Seattle Children's Research Institute. His research in the laboratory is focused on two broad areas. First, he studies the mechanisms responsible for breaking B cell tolerance during the development of autoimmunity. Second, he has developed an interest in B cell-mediated acceleration of atherosclerosis in autoimmune disease.

    • will Yakima, Wa 08.29.12

      Dr. Jackson has been instrumental in our daughter recovey and maintenance of her illness. He is personable and does a thorough job on making sure our questions are answered and we understand all the medical jargon and research. Lastly, he is a friendly and compassionate person.

  • Award Name Award Description Awarded By Award Date
    Trainee/Young Investigator Top Abstract award American Society of Nephrology (ASN) Annual Kidney Week. Nov. 2015
    Postdoctoral fellow poster prize University of Washington Immunology department annual retreat 2013
    Outstanding Presentation Award Seattle Childrens Fellow and Resident Research Day April 2012
    Distinguished Fellow Award American College of Rheumatology (ACR) 2012
    Fellow teaching award Seattle Children's Hospital June 2009
    Best oral presentation, Young Investigator Award Session Asia Pacific Association for the Study of the Liver Feb. 2004
    University Gold Medal For the most distinguished student in the graduating MBChB class University of Cape Town Dec. 2001
  • Other Publications

    • Kolhatkar NS, Scharping NE, Sullivan JM, Jacobs HM, Schwartz MA, Khim S, Notarangelo LD, Thrasher AJ, Rawlings DJ, Jackson SW
      B-cell intrinsic TLR7 signals promote depletion of the marginal zone in a murine model of Wiskott-Aldrich syndrome.
      26256668 European journal of immunology, 2015 Oct. : 45(10)2773-9 PMCID:PMC4679197
    • Jackson SW, Kolhatkar NS, Rawlings DJ
      B cells take the front seat: dysregulated B cell signals orchestrate loss of tolerance and autoantibody production.
      25679954 Current opinion in immunology, 2015 Feb. 10 : 33C70-77
    • 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.
      23619366 The Journal of clinical investigation, 2013 May : 123(5)2024-36 PMCID:PMC3638909
    • Rawlings DJ, Schwartz MA, Jackson SW, Meyer-Bahlburg A
      Integration of B cell responses through Toll-like receptors and antigen receptors.
      22421786 Nature reviews. Immunology, 2012 March 16 : 12(4)282-94 PMCID:PMC3437941
    • Rawlings DJ, Schwartz MA, Jackson SW, Meyer-Bahlburg A
      Integration of B cell responses through Toll-like receptors and antigen receptors.
      22421786 Nature reviews. Immunology, 2012 March 16 : 12(4)282-94
    • Allen JL, Flick LM, Divanovic S, Jackson SW, Bram R, Rawlings DJ, Finkelman FD, Karp CL
      Cutting edge: regulation of TLR4-driven B cell proliferation by RP105 is not B cell autonomous.
      22291190 Journal of immunology (Baltimore, Md. : 1950), 2012 March 1 : 188(5)2065-9 PMCID:PMC3288200
    • Becker-Herman S, Meyer-Bahlburg A, Schwartz MA, Jackson SW, Hudkins KL, Liu C, Sather BD, Khim S, Liggitt D, Song W, Silverman GJ, Alpers CE, Rawlings DJ
      WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.
      21875954 The Journal of experimental medicine, 2011 Sept. 26 : 208(10)2033-42 PMCID:PMC3182055
    • Jackson SW
      Hypernatremia, Hyponatremia, Hyperkalemia, Hypokalemia, Renal Tubular Acidosis
      POCKET PEDIATRICS, 2nd edition, 2009
    • Jackson SW, Hoshi T, Wu Y, Sun X, Enjyoji K, Cszimadia E, Sundberg C, Robson SC
      Disordered purinergic signaling inhibits pathological angiogenesis in cd39/Entpd1-null mice.
      17823293 The American journal of pathology, 2007 Oct. : 171(4)1395-404 PMCID:PMC1988887

  • Presentations Title Event Location Date
    B Cell-Intrinsic Interferon Gamma Signals Promote the Development of Systemic Lupus Erythematosus By Enhancing the Formation of Spontaneous Autoimmune Germinal Centers American College of Rheumatology (ACR) annual meeting San Francisco, CA Nov. 2015
    B Cell-Intrinsic Interferon Gamma (IFN-) Signals Promote B Cell Activation and the Development of Lupus Nephritis American Society of Nephrology (ASN) Kidney Week San Diego, CA Nov. 2015
    The B Cell Survival Cytokine BAFF Promotes Systemic Lupus Erythematosus Via Activation of TACI, Not BAFF Receptor American College of Rheumatology (ACR) annual meeting San Francisco, CA Nov. 2015
    The B Cell Survival Cytokine BAFF Promotes Murine Lupus Nephritis via Activation of TACI, Not BAFF Receptor. American Society of Nephrology (ASN) Kidney Week San Diego, CA Nov. 2015
    B Cell-Intrinsic Deletion of the Type 1 Interferon Receptor Does Not Impact the Development of Murine Lupus. American College of Rheumatology (ACR) annual meeting Boston, MA Nov. 2014
    Opposing impact of B cell intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation. Pediatric Academic Societies (PAS) Vancouver, BC, CA May 2014
    Trypanosoma cruzi trans-sialidase initiates an ROR-t independent program leading to high-level IL-17 production by activated B cells. Keystone Symposium, "B Cell Development and Function". Keystone, CO Feb. 2013
    Marginal zone defects in Wiskott-Aldrich syndrome are dependent on B cell intrinsic TLR signals. Federation of Clinical Immunology Societies meeting (FOCIS 2012) Vancouver, BC June 2012
    Renal transplantation from a donor with undiagnosed Class V lupus nephritis demonstrates prolonged histopathologic features of lupus nephritis despite absence of SLE in recipients. Pediatric Rheumatology Symposium (PRSyM) Miami, FL June 2011
    Decreased activity of endothelial V3 integrin in the Cd39-null mouse is associated with defective tumor angiogenesis. 4th International Symposium of Nucleosides and Nucleotides.Purines 2004 Chapel Hill, NC 2004
    Disordered Liver Regeneration and Defective Angiogenesis in NTPDase1/Cd39-Null Mice. Young Investigator Award Session. Asia Pacific Association for the Study of the Liver Delhi, India 2004
  • Grant Title Grantor Amount Award Date
    Pediatric Early Research Career (PERC) award Seattle Children's Research Institute $150,000 July 1, 2015 - Sept. 30, 2016
    Mentored Clinical Scientist Research Career Development Award (K08) NIH/NIAID $177,250/year July 1, 2014 - June 30, 2019


Board Certification(s)

Pediatric Rheumatology
Pediatric Nephrology

Medical/Professional School

University of Cape Town, Rodebosch, Cape Town


Pediatrics, Boston Children's Hospital, Boston


Nephrology, University of Washington, Seattle
Rheumatology, University of Washington, Seattle

Clinical Interests

My clinical interests are in the diagnosis and management of infants, children and adolescents with renal and rheumatologic diseases. In particular, my focus is on those autoimmune conditions at the interface of nephrology and rheumatology, especially systemic lupus erythematosus (SLE) and systemic vasculitis.

Research Description

My research interests in the laboratory relate to basic cellular mechanisms that underlie B cell mediated autoimmunity. In particular, we study the why B cells break tolerance and develop reactivity to self in systemic autoimmune disease, for example in systemic lupus erythematosus (SLE). In addition, as accelerated cardiovascular disease is a major cause of morbidity in patients with autoimmune diseases, including SLE and rheumatoid arthritis, we are studying the B cells mechanisms responsible for accelerated atherosclerosis in autoimmune settings.