Molecular and Genetic Determinants of iNKT Cell Function
Dr. Boyson received his PhD from the University of Wisconsin-Madison in 1997. From 1998 to 2003, he conducted his postdoctoral research at Harvard University in the Department of Molecular and Cellular Biology in the laboratory of Dr. Jack L. Strominger. Dr. Boyson joined the CMB program in 2003.
Semi-invariant NKT cells comprise an unusual, highly conserved, lymphocyte subset that has been implicated in tolerance induction, tumor immunology, autoimmunity, and infectious disease. Unlike most T cells which recognize peptide bound by class I MHC molecules, iNKT cells bind glycolipids bound by the class I MHC-like molecule CD1d. Upon activation, NKT cells produce both Th1 (e.g., IFN-gamma and TNF-alpha) as well as Th2 (e.g., IL-4, IL-10, and IL-13) cytokines. Accordingly, they have been observed to play roles in both pro-inflammatory as well as tolerogenic immune responses. Rapid production by NKT cells of a wide variety of cytokines elicits the downstream activation of both innate and adaptive immune cell subsets such as NK cells, macrophages, dendritic cells, and B cells. These characteristics suggest that NKT cells could play a pivotal early role in shaping developing immune responses.
Research in the lab focuses on the investigation of the factors that govern iNKT cell activation and function. We have demonstrated strain-dependent susceptibility to NKT-mediated diseases such as asthma and pregnancy loss is significantly correlated with strain-dependent variability in iNKT cell number and function. Therefore, we are using genetic, molecular, and biochemical techniques to identify factors that modulate iNKT cell function in vivo, and to determine how they affect downstream immune responses.
Nagaleekar, V., G. Sabio, I. Aktan, A. Chant, I.W. Howe, P.J. Benoit, T.M. Thornton, R.J. Davis, M. Rincon, and J.E. Boyson. Translational control of NKT cell cytokine production by p38 MAP kinase. 2011. Journal of Immunology 186(7):4140-4146.
Exley, M.A. and J.E. Boyson. Protective role of regulatory decidual γδ T cells in pregnancy. 2011. Clinical Immunology 141:236–239.
Ather JL, Ckless K, Martin R, Foley KL, Suratt BT, Boyson JE, Fitzgerald KA, Flavell RA, Eisenbarth SC, Poynter ME. Serum Amyloid A Activates the NLRP3 Inflammasome and Promotes Th17 Allergic Asthma in Mice. 2011. Journal of Immunology 187(1):64-73.
Paveglio SA, Allard J, Foster Hodgkins SR, Ather J, Bevelander M, Mayette Campbell J, Whittaker Leclair LA, McCarthy SM, van der Vliet A, Suratt BT, Boyson JE, Uematsu S, Akira S, Poynter ME. Airway Epithelial Indoleamine 2,3-Dioxygenase Inhibits CD4+ T Cells During Aspergillus fumigatus Antigen Exposure. 2011. Am J Respir Cell Mol Biol 44(1):11-23.
Aktan, I, Chant, AC, Borg, ZD, Damby, DE, Leenstra, PC, Lilley, GWJ, Petty, J, Suratt, BT, Teuscher, C., Wakeland, EK, Poynter, ME, and JE Boyson. Slam haplotypes modulate the response to LPS in vivo through control of NKT cell number and function. 2010. Journal of Immunology 185(1):144-56.
Hodgkins, S.R., J. L. Ather, S.A. Paveglio, J.L. Allard, L.A. Whittaker LeClair, B.T. Suratt, J.E. Boyson, and M.E. Poynter. NO2 Inhalation Induces Maturation of Pulmonary CD11c+ Cells that Promote Antigen-Specific CD4+ T Cell Polarization. 2010. Respir Res 11(1): p. 102.
Olson CM Jr, Bates TC, Izadi H, Radolf JD, Huber SA, Boyson JE, Anguita J. Local production of IFN-gamma by invariant NKT cells modulates acute lyme carditis. 2009. Journal of Immunology 182(6):3728-34.
* indicates equal contribution
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