Nicholas Arpaia, PhD

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Dr. Arpaia received a B.S. in Biochemistry from SUNY Geneseo in 2006 and went on to work in the laboratory of Dr. Gregory M. Barton in the Department of Molecular and Cell Biology at the Univeristy of California, Berkeley where he received a Ph.D. in Immunology and Pathogenesis in 2011. He later joined the laboratory of Dr. Alexander Y. Rudensky at Memorial Sloan Kettering Cancer Center where he completed a Postdocotoral Fellowship studying Molecular Immunology in 2016. Dr. Arpaia joined the Department of Microbiology & Immunology at Columbia University Medical Center as an Assistant Professor in September of 2016.


  • Italian

Credentials & Experience

Education & Training

  • BS, 2006 Biochemistry, State University of New York at Geneseo
  • PhD, 2011 Immunology and Pathogenesis, University of California, Berkeley

Honors & Awards

Searle Scholar (2017)

Tri-Institutional Breakout Prize, Memorial Sloan Kettering/Rockefeller University/Weill Cornell (2016)

Damon Runyon Cancer Research Foundation Robert Black Postdoctoral Fellow (2013)


Immunity and tolerance are achieved by balancing pro- and anti-inflammatory responses to limit or prevent collateral tissue damage while neutralizing an invading pathogen. At mucosal barriers — which are colonized by diverse communities of commensal microbes and serve to interface the internal physiology of an organism with the ever-changing external environment — fine-tuning opposing immune responses is of even greater relevance. Constant exposure to novel environmental molecules and high concentrations of microbial products that can activate innate immunity increase the risk for persistent inflammatory activation. As a result, complex immune networks operate to contextualize diverse microbial and environmental stimuli. These inputs subsequently shape mucosal immune responses and synergize to preserve mucosal barrier integrity and function. Aberrant immune responses, due to a breakdown in tolerance or defects in barrier maintenance, largely underlie the etiology of chronic mucosal inflammatory disorders.

Our laboratory is committed to understanding how mucosal immune responses are coordinated to maintain homeostasis and respond to microbial infection, barrier disruption, or alterations in commensal microbial diversity — with an emphasis on how these molecular decisions are balanced within the context of host fitness and organ physiology. Our studies are geared toward uncovering pathways with the potential for therapeutic manipulation, focusing on the signals that drive pro- and anti-inflammatory immune responses within each setting. To pursue these goals, we are exploring the molecular mechanisms underlying epithelial barrier repair and investigating the contribution of commensal microbial colonization in these processes.

Research Interests

  • Host-microbe interactions
  • Immunometabolism
  • Mucosal immunity
  • Tissue repair

Selected Publications

  1. Green, J.A.*, Arpaia, N.*, Schizas, M., Dobrin, A., Rudensky, A.Y. (2017) A nonimmune function of T cells in promoting lung tumor progression. J. Exp. Med. doi:10.1084/jem.20170356. [Epub ahead of print].
  2. Arpaia, N., Green, J.A., Moltedo, B., Arvey, A., Hemmers, S., Yuan, S., Treuting, P.M. and Rudensky, A.Y. (2015) A distinct function of regulatory T cells in tissue protection. Cell 162:1078-1089.
  3. Jenq, R.R., Taur, Y., Devlin, S.M., Ponce, D.M., Goldberg, J.D., Ahr, K.F., Littmann, E.R., Ling, L., Gobourne, A.C., Miller, L.C., Docampo, M.D., Peled, J.U., Arpaia, N., Cross, J.R., Peets, T.K., Lumish, M.A., Shono, Y., Dudakov, J.A., Poeck, H., Hanash, A.M., Barker, J.N., Perales, M.A., Giralt, S.A., Pamer, E.G. and van den Brink M.R. (2015) Intestinal Blautia is associated with reduced death from graft-versus-host disease. Biol. Blood Marrow Transplant 21: 1373-1383.
  4. Arpaia, N. (2014) Keeping peace with the microbiome: acetate dampens inflammatory cytokine production in intestinal epithelial cells. Immunol. Cell Biol. 92: 561-562.
  5. Sivick, K.E., Arpaia, N., Shu, J. and Barton, G.M. (2014) Toll-like receptor deficient mice reveal how innate immune signaling influences Salmonella virulence strategies. Cell Host and Microbe 15: 203-213.
  6. Arpaia, N. and Rudensky, A.Y. (2014) Microbial metabolites control gut inflammatory responses. Proc. Natl. Acad. Sci. U.S.A. 111: 2058-2059.
  7. Arpaia, N., Campbell, C., Fan, X., Dikiy, S., van der Veeken, J., deRoos, P., Liu, H., Cross, J.R., Pfeffer, K., Coffer, P.J. and Rudensky, A.Y. (2013) Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature 504: 451-455.
  8. Arpaia, N. and Barton, G.M. (2013) The impact of Toll-like receptors on bacterial virulence strategies. Curr. Opin. Microbiol. 16: 17-22.
  9. Mouchess, M.L., Arpaia, N., Souza, G., Barbalat, R., Ewald, S.E., Lau, L. and Barton, G.M. (2011) Transmembrane mutations in toll-like receptor 9 bypass the requirement for ectodomain proteolysis and induce fatal inflammation. Immunity 35: 1-12.
  10. Arpaia, N. and Barton, G.M. (2011) Toll-like receptors: key players in antiviral immunity. Curr. Opin. Virol. 1: 1-8.
  11. Arpaia, N., Godec, J., Lau, L., Sivick, K.E., McLaughlin, L.M., Jones, M.B., Dracheva, T., Peterson, S.N., Monack, D.M. and Barton, G.M. (2011) TLR signaling is required for Salmonella typhimurium virulence. Cell 144: 675-688.