University of Vermont

College of Medicine

Vermont Center for Immunobiology and Infectious Diseases

Bio for Jonathan Boyson, Ph.D.
Jonathan Boyson, Ph.D.

Jonathan Boyson, Ph.D.

Associate Professor of Surgery
Roger G. Allbee Professor of Surgery
Vice Chair of Research
Chief, Division of Surgical Research

Contact Information
Office Location:
Given D319-D, 89 Beaumont Ave., Burlington, VT 05405


Program in Cellular and Molecular Biology, University of Wisconsin at Madison, Madison, WI (1997)
Post-doctoral Fellow
Wisconsin Regional Primate Research Center, University of Wisconsin – Madison, Madison, WI  (1998)
Post-doctoral Fellow
Molecular and Cellular Biology, Harvard University, Cambridge, MA (2003)

Research Interests

A host genetic locus that regulates susceptibility to influenza infection
Susceptibility to infectious disease is one of the most strongly inherited of all common disease traits. Yet, we still do not have a clear understanding of how host genetic regulation of the immune response ultimately affects disease outcome. Slam genes comprise a family of tightly linked genes that encode costimulatory/adhesion molecules that transduce signals through association with the cytosolic adapter protein, SLAM-associated protein (SAP). Mutations in the gene encoding SAP (Sh2d1a) results in the development of a serious immunodeficiency that often results in mortality due to virus infection, highlighting the central role that the Slam/SAP signaling pathway plays in the host response to viral pathogens. Slam genes are polymorphic in humans and in mice, and these polymorphisms have been linked to the development of autoimmunity. However, despite the significant role that the Slam/SAP signaling pathway plays in the host response to virus infection, there has been almost no study of the potential contribution of Slam locus polymorphisms to susceptibility to virus infection.

            We are studying the contribution of naturally occurring genetic variation at the Slam locus to host susceptibility to influenza infection. Our preliminary data indicates that one or more genes within this locus regulates susceptibility to influenza infection, and that mortality is associated with an increase in IL-17A-producing gd T cells in the lung. Our working hypothesis is that genetic variation at one or more Slam genes regulates susceptibility to virus infection through regulation of gd T cell and/or NKT cell function.

The function of Slamf6 on NKT cells
            Slamf6 (Ly108) and Slamf1 have previously been demonstrated to be critical in NKT cell development. In mice that are only deficient in Slamf6, NKT cells develop, but there are fewer of them, and their numbers are particularly low in the liver. In addition, it has been demonstrated that the absence of NKT cells in SAP-deficient mice is due to negative signaling from the Slamf6 receptor. However, the exact nature of the function of Slamf6 on NKT cells in the periphery is still unclear. We are utilizing Slamf6-deficient mice (a gift from Pam Schwartzberg) and B6.129 congenic strains in which a 129X1/SvJ-derived region encompassing the Slam genes has been introgressed onto the C57BL/6J background to investigate this question.

Immune correlates of protection in a candidate Dengue virus vaccine trial
            Dengue virus infection constitutes a significant global health problem, and numerous efforts are underway to develop an effective vaccine. We are collaborating with Beth Kirkpatrick MD and Sean Diehl PhD in the University of Vermont Vaccine Testing Center, and Jason Botten PhD in the Dept. of Medicine to evaluate immune correlates of protection in a candidate live attenuated tetravalent vaccine developed at the NIH. Using dengue-specific MHC class I peptide pools provided by Alex Sette PhD and Daniela Weiskopf PhD at the La Jolla Institute for Allergy and Immunology (LIAI), we are evaluating the breadth and magnitude of the CD8+ and CD4+ T cell responses in a human challenge model of dengue vaccination.


Benoit, P, Sigounas VY, Thompson JL, van Rooijen N, Poynter ME, Wargo MJ, Boyson JE. The role of CD1d-restricted NKT cells in the clearance of Pseudomonas aeruginosa from the lung is dependent on the host genetic background. Infect Immun. 2015. 83(6):2557-65.

Ather JL, Foley KL, Suratt BT, Boyson JE, Poynter ME. Airway epithelial NF-kB activation promotes the ability to overcome inhalational antigen tolerance.  Clin Exp Allergy. 2015 Jan 23. doi: 10.1111/cea.12491. [Epub ahead of print]

Borg ZD, Benoit PJ, Lilley GW, Aktan I, Chant A, DeVault VL, Rincon M, Boyson JE. Polymorphisms in the CD1d promoter that regulate CD1d gene expression are associated with impaired NKT cell development.  J Immunol. 2014 Jan 1;192(1):189-99.

Klaus JP, Eisenhauer P, Russo J, Mason AB, Do D, King B, Taatjes D, Cornillez-Ty C, Boyson JE, Thali M, Zheng C, Liao L, Yates JR 3rd, Zhang B, Ballif BA, Botten JW. The intracellular cargo receptor ERGIC-53 is required for the production of infectious arenavirus, coronavirus, and filovirus particles. Cell Host Microbe. 2013 Nov 13;14(5):522-34.

Liu W, Moussawi M, Roberts B, Boyson JE, Huber SA. Cross-Regulation of T Regulatory Cell Response after Coxsackievirus B3 Infection by NKT and ?d T Cells in the Mouse. Am J Pathol. 2013 Aug;183(2):441-9.

Martin RA, Ather JL, Lundblad LK, Suratt BT, Boyson JE, Budd RC, Alcorn JF, Flavell RA, Eisenbarth SC, Poynter ME. Interleukin-1 receptor and caspase-1 are required for the Th17 response in nitrogen dioxide-promoted allergic airway disease. Am J Respir Cell Mol Biol. 2013 May;48(5):655-64.

Huber SA, Roberts B, Moussawi M, Boyson JE. Slam haplotype 2 promotes NKT but suppresses v?4(+) T-cell activation in coxsackievirus b3 infection leading to increased liver damage but reduced myocarditis. Am J Pathol. 2013;182(2):401-9.

Exley M.A., Boyson J.E.. Protective role of regulatory decidual gd T cells in pregnancy. Clin Immunol  2011;141:236–239.

Ather, J.L., K. Ckless, R. Martin, K.L. Foley, B.T. Suratt, J.E. Boyson, K.A. Fitzgerald, R A. Flavell, S.C. Eisenbarth, and M.E. Poynter. Serum Amyloid A Activates the NLRP3 Inflammasome and Promotes Th17 Allergic Asthma in Mice. J Immunol  2011;187(1): 64-73.

Nagaleekar V, Sabio G, Aktan I, Chant A, Howe IW, Thornton TM, Beniot PJ, Davis RJ, Rincon M, Boyson JE. Regulation of NKT cell cytokine production in NKT cells by p38 MAP kinase. J Immunol  2011;186(7):4140-4146.

Paveglio S,  Allard J, Foster S, Ather J, Bevelander M, Mayette J, Whittaker L, Boyson JE, Poynter ME. Airway epithelial indoleamine 2,3, -dioxygenase inhibits CD4+ T cells during Aspergillus fumigatus antigen exposure.  Am J Respir Cell Mol Biol. 2011;44(1):11-23.

Publications in Pubmed