Matthew Jones, PhD

Faculty and Fellows

Associate Professor of Medicine

Graduate Education: Boston University School of Medicine, PhD, 2003, Vascular biology
Other Post-doctoral Fellowship: Harvard School of Public Health (Joseph Mizgerd)

Special Interests:


  • Post-transcriptional gene regulation
  • Innate immunity in the lungs

Our research is broadly focused on the host inflammatory response to acute bacterial pneumonia. During pneumonia, various pro-inflammatory cytokines and chemokines are released to guide immune cells to the site of infection. Too much inflammation can compromise normal lung function whereas, too little of a host response can lead to uncontrolled bacterial growth and sepsis. Cytokine expression thus needs to be carefully directed by molecular mechanisms regulating transcription, mRNA stability, and translation. Our work is centered on several aspects of cytokine mRNA instability. In general, cytokine transcripts are very labile which is a property imparted by various sequence elements residing in their 3´ untranslated regions (UTRs). These 3´ UTRs contain AU-rich elements (AREs) that are bound by ARE-binding proteins and direct mRNA translational efficiency and decay. One project in the lab is centered on how specific ARE-binding proteins regulate select cytokine expression during inflammation. In addition to AREs, many cytokine transcript 3´ UTRs are targeted by microRNAs, which can lead to their abrogated translation, deadenylation, and ultimately, decay. Another research focus of ours is exploring how cytokine transcript targeting microRNAs themselves are processed and regulated. We have found that the Zcchc11 protein is a uridyltransferase that is responsible for the uridylation of specific microRNAs. End modifications of microRNAs, such as untemplated uridylation, can reduce their ability to repress the targeted transcript. Future studies are designed to elucidate which microRNAs are modified by Zcchc11 during inflammation and whether these edits have functional consequences. Understanding how these mechanisms function to orchestrate inflammation during pneumonia will provide an important basis for future disease management.

Selected Publications:

  1. Jones MR, Quinton LJ, Blahna MT, Neilson JR, Fu S, Ivanov AR, Wolf DA, Mizgerd JP. Zcchc11-dependent uridylation of microRNA directs cytokine expression. Nat. Cell. Biol. 2009 Sep; 11(9): 1157-63
  2. Quinton LJ, Jones MR, Robson BE, Simms BT, Uematsu S, Akira S, Whitsett JA, Mizgerd JP. Alveolar epithelial STAT3 activation depends on IL-6 family cytokines, mediates host defense, and prevents lung injury during Escherichia coli pneumonia. Amer. J. Resp. Cell Mol. Bio. 2008 Jan 10.
  3. Quinton LJ, Jones MR, Simms BT, Kogan MS, Robson BE, Wilson CB, Skerrett SJ, and Mizgerd JP. Functions and regulation of NF-kB RelA during pneumococcal pneumonia. J. Immunol. 2007 Feb 1;178(3):1896-903.
  4. Yang D, Zhang Y, Nguyen HG, Koupenova M, Chauhan AK, Makitalo M, Jones MR, Hilaire CS, Seldin DC, Toselli P, Lamperti E, Schreiber BM, Gavras H, Wagner DD, Ravid K. The A(2B) adenosine receptor protects against inflammation and excessive vascular adhesion. J Clin Invest. 2006 Jul 3;116(7):1913-1923.
  5. Jones MR, Quinton LJ, Simms BT, Lupa MM, Kogan MS, and Mizgerd JP. Roles of interleukin-6 in STAT activation and neutrophil recruitment during Escherichia coli pneumonia. J Infect Dis. 2006 Feb 1;193(3):360-9.
  6. Jones MR, Simms BT, Lupa MM, Kogan MS, and Mizgerd JP. Lung NF-kB activation and neutrophil recruitment require IL-1 and TNF receptor signaling during pneumococcal pneumonia. J Immunol. 2005 Dec 1;175(11):7530-5.