Medical School

  • Harvard Medical School , 1997 , Boston , MA


  • Brigham & Women's Hospital , 1998 , Boston , MA


  • Brigham & Women's Hospital , 1999 , Boston , MA


  • Brigham & Women's Hospital/Massachusetts General Hospital , 2003 , Boston , MA

Philosophy of Care

I came to Boston Children’s Hospital with a commitment to promoting the health and well-being of children by advancing the clinical and research missions of the Division of Infectious Diseases.


Dennis Kim, M.D., Ph.D., is Chief of the Division of Infectious Diseases at Boston Children’s Hospital. He received his undergraduate education at the University of California at Berkeley, and his medical and graduate degrees at Harvard Medical School. He completed his internship and residency in Internal Medicine at the Brigham and Women’s Hospital, and subspecialty training in Infectious Diseases from the combined program at the Massachusetts General Hospital and Brigham and Women’s Hospital. He is a Fellow of the Infectious Disease Society of America. Prior to assuming his current position at Boston Children’s Hospital, for thirteen years Dr. Kim served as a Professor in the Department of Biology at the Massachusetts Institute of Technology, while also maintaining clinical attending responsibilities in Infectious Diseases at the Massachusetts General Hospital.


  • American Board of Internal Medicine, Infectious Diseases


Publications powered by Harvard Catalyst Profiles

  1. Host-microbe interactions and the behavior of Caenorhabditis elegans. J Neurogenet. 2020 Sep-Dec; 34(3-4):500-509. View abstract
  2. Immediate activation of chemosensory neuron gene expression by bacterial metabolites is selectively induced by distinct cyclic GMP-dependent pathways in Caenorhabditis elegans. PLoS Genet. 2020 08; 16(8):e1008505. View abstract
  3. Population Density Modulates the Duration of Reproduction of C. elegans. Curr Biol. 2020 07 06; 30(13):2602-2607.e2. View abstract
  4. Global transcriptional regulation of innate immunity by ATF-7 in C. elegans. PLoS Genet. 2019 02; 15(2):e1007830. View abstract
  5. Endoplasmic Reticulum Homeostasis Is Modulated by the Forkhead Transcription Factor FKH-9 During Infection of Caenorhabditis elegans. Genetics. 2018 12; 210(4):1329-1337. View abstract
  6. Bacterial Siderophores Promote Animal Host Iron Acquisition and Growth. Cell. 2018 10 04; 175(2):311-312. View abstract
  7. Signaling in the innate immune response. WormBook. 2018 08 14; 2018:1-35. View abstract
  8. PDF-1 neuropeptide signaling regulates sexually dimorphic gene expression in shared sensory neurons of C. elegans. Elife. 2018 07 19; 7. View abstract
  9. Molecular Determinants of the Regulation of Development and Metabolism by Neuronal eIF2a Phosphorylation in Caenorhabditis elegans. Genetics. 2017 05; 206(1):251-263. View abstract
  10. Sexually dimorphic control of gene expression in sensory neurons regulates decision-making behavior in C. elegans. Elife. 2017 01 24; 6. View abstract
  11. Age-Dependent Neuroendocrine Signaling from Sensory Neurons Modulates the Effect of Dietary Restriction on Longevity of Caenorhabditis elegans. PLoS Genet. 2017 01; 13(1):e1006544. View abstract
  12. Mutations in Nonessential eIF3k and eIF3l Genes Confer Lifespan Extension and Enhanced Resistance to ER Stress in Caenorhabditis elegans. PLoS Genet. 2016 09; 12(9):e1006326. View abstract
  13. IRE1 Sulfenylation by Reactive Oxygen Species Coordinates Cellular Stress Signaling. Mol Cell. 2016 08 18; 63(4):541-542. View abstract
  14. Inhibition of Lithium-Sensitive Phosphatase BPNT-1 Causes Selective Neuronal Dysfunction in C. elegans. Curr Biol. 2016 07 25; 26(14):1922-8. View abstract
  15. Signal Transduction: A Different Kind of Toll Is in the BAG. Curr Biol. 2015 Aug 31; 25(17):R767-9. View abstract
  16. Tissue expression pattern of PMK-2 p38 MAPK is established by the miR-58 family in C. elegans. PLoS Genet. 2015 Feb; 11(2):e1004997. View abstract
  17. Chemosensation of bacterial secondary metabolites modulates neuroendocrine signaling and behavior of C. elegans. Cell. 2014 Oct 09; 159(2):267-80. View abstract
  18. Behavioral avoidance of pathogenic bacteria by Caenorhabditis elegans. Trends Immunol. 2014 Oct; 35(10):465-70. View abstract
  19. The unfolded protein response in a pair of sensory neurons promotes entry of C. elegans into dauer diapause. Curr Biol. 2013 Dec 16; 23(24):2540-5. View abstract
  20. Bacteria and the aging and longevity of Caenorhabditis elegans. Annu Rev Genet. 2013; 47:233-46. View abstract
  21. Physiological IRE-1-XBP-1 and PEK-1 signaling in Caenorhabditis elegans larval development and immunity. PLoS Genet. 2011 Nov; 7(11):e1002391. View abstract
  22. Natural polymorphisms in C. elegans HECW-1 E3 ligase affect pathogen avoidance behaviour. Nature. 2011 Nov 16; 480(7378):525-9. View abstract
  23. Caenorhabditis elegans NPR-1-mediated behaviors are suppressed in the presence of mucoid bacteria. Proc Natl Acad Sci U S A. 2011 Aug 02; 108(31):12887-92. View abstract
  24. A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans. PLoS Genet. 2011 May; 7(5):e1002082. View abstract
  25. Phosphorylation of the conserved transcription factor ATF-7 by PMK-1 p38 MAPK regulates innate immunity in Caenorhabditis elegans. PLoS Genet. 2010 Apr 01; 6(4):e1000892. View abstract
  26. An essential role for XBP-1 in host protection against immune activation in C. elegans. Nature. 2010 Feb 25; 463(7284):1092-5. View abstract
  27. Tissue-specific activities of an immune signaling module regulate physiological responses to pathogenic and nutritional bacteria in C. elegans. Cell Host Microbe. 2009 Oct 22; 6(4):321-30. View abstract
  28. The G protein-coupled receptor FSHR-1 is required for the Caenorhabditis elegans innate immune response. Proc Natl Acad Sci U S A. 2009 Feb 24; 106(8):2782-7. View abstract
  29. A polymorphism in npr-1 is a behavioral determinant of pathogen susceptibility in C. elegans. Science. 2009 Jan 16; 323(5912):382-4. View abstract
  30. Studying host-pathogen interactions and innate immunity in Caenorhabditis elegans. Dis Model Mech. 2008 Nov-Dec; 1(4-5):205-8. View abstract
  31. Transcriptional responses to pathogens in Caenorhabditis elegans. Curr Opin Microbiol. 2008 Jun; 11(3):251-6. View abstract
  32. p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans. PLoS Genet. 2006 Nov 10; 2(11):e183. View abstract
  33. Evolutionary perspectives on innate immunity from the study of Caenorhabditis elegans. Curr Opin Immunol. 2005 Feb; 17(1):4-10. View abstract
  34. Integration of Caenorhabditis elegans MAPK pathways mediating immunity and stress resistance by MEK-1 MAPK kinase and VHP-1 MAPK phosphatase. Proc Natl Acad Sci U S A. 2004 Jul 27; 101(30):10990-4. View abstract
  35. The Caenorhabditis elegans MAPK phosphatase VHP-1 mediates a novel JNK-like signaling pathway in stress response. EMBO J. 2004 Jun 02; 23(11):2226-34. View abstract
  36. Requirement for a conserved Toll/interleukin-1 resistance domain protein in the Caenorhabditis elegans immune response. Proc Natl Acad Sci U S A. 2004 Apr 27; 101(17):6593-8. View abstract
  37. Long-lived C. elegans daf-2 mutants are resistant to bacterial pathogens. Science. 2003 Jun 20; 300(5627):1921. View abstract
  38. A conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity. Science. 2002 Jul 26; 297(5581):623-6. View abstract