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Kevin Nickerson Ph.D.

  • Research Assistant Professor, Department of Immunology

    Education & Training

  • Postdoc - Yale University
  • Ph.D. - University of Michigan
  • B.S. - Yale University
Representative Publications

Nickerson KM, Smita S, Hoehn KB, Marinov AD, Thomas KB, Kos JT, Yang Y, Bastacky SI, Watson CT, Kleinstein SH, and Shlomchik MJ. (2023) "Age-associated B cells are heterogeneous and dynamic drivers of autoimmunity in mice."  J. Exp. Med. 220(5) e20221346.  doi:10.1084/jem.20221346

Leibler C, John S, Elsner RA, Thomas KB, Smita S, Joachim S, Levack RC, Callahan DJ, Gordon RA, Bastacky S, Fukui R, Miyake K, Gingras S, Nickerson KM, and Shlomchik MJ. (2022) "Genetic dissection of TLR9 reveals complex regulatory and cryptic proinflammatory roles in mouse lupus." Nat. Immunol. 23(10):1457-1469.  doi:10.1038/s41590-022-01310-2

Tilstra JS, John S, Gordon RA, Leibler C, Kashgarian M, Bastacky S, Nickerson KM, and Shlomchik MJ. (2020) "B cell-intrinsic TLR9 expression is protective in murine lupus." J. Clin. Invest. 130(6):3172-3187.  doi:10.1172/JCI132328

Nickerson KM, Wang Y, Bastacky S, Shlomchik MJ. (2017) "Toll-like receptor 9 suppresses lupus disease in Fas-sufficient MRL Mice."  PLoS ONE 12(3):e0173471.  doi:10.1371/journal.pone.0173471

Nickerson KM and Shlomchik MJ.  (2016)  "Animal Models of Autoimmunity"  In: Ratcliffe, MJH (ed.) Encyclopedia of Immunobiology. Oxford: Academic Press; Vol 5, p. 227-40.

Complete List of Publications

Research Interests
  • B cell tolerance
  • Systemic lupus erythematosus

As a member of Dr. Shlomchik's research group, my research focuses on B cell tolerance in systemic autoimmunity (lupus) including how B cells are regulated by the Toll-like receptors, TLR7 and TLR9.  Recently we have been working on a subset of B cells sometimes called "age-associated B cells" (ABCs) which are expanded in human patients with lupus and in mouse models of that disease.  ABCs are thought to be a form of autoimmune memory B cell and the precursor to autoantibody-forming plasmablasts.  Using genetic tools in the MRL/lpr model, we showed that ABC-like cells in the MRL/lpr model are heterogeneous with respect to expression of integrins CD11c and CD11b, T-bet, and memory and plasmablast markers.  We showed that these cells, unlike conventional memory B cells, are undergoing continual cycles of proliferation, mutation and differentiation.  Depletion of CD11c+ B cells improved lupus disease in this model, making them an attractive target for future therapeutic approaches.