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Nikki M. Heller, PhD

Dr. Nicola Heller

   Assistant Professor
   Department of Anesthesiology/Critical Care Medicine

   The Johns Hopkins University School of Medicine
   720 Rutland Avenue, Ross 367
   Baltimore, MD 21205
   Phone: (410) 955-1743
   Fax: (410) 614-0083



Research Interests

The focus of Dr. Heller's laboratory is the role of IL-4/IL-13 signaling in asthma and allergic disease. She is interested in the basic mechanisms of signaling: from the biology, signal transduction, and regulation of the IL-4/IL-13 receptor to the role of alternatively activated macrophages in the pathogenesis of allergic inflammation. Alternatively activated macrophages, or AAM, differentiate from resting macrophages in the presence of IL-4 or IL-13 and are involved in mediating Th2-type inflammation, such as immune responses to helminth worms and allergens. Their phenotype contrasts with “classically activated” or “inflammatory” macrophages. AAM are considered “anti-inflammatory” in that they are thought to suppress inflammatory reactions to control worm infection or inflammatory responses to allergens. AAM contain inflammation by promoting fibrosis through release of chitinase-like molecules, inducing regulatory T-cells (Tregs), dampening T-cell responses, and producing anti-inflammatory cytokines, such as IL-10. However, when these AAM responses become chronic or are dysregulated, they can result in pathogenesis as seen in lung fibrosis and asthma.

It is becoming increasingly clear that the balance between alternatively activated and classically activated macrophages centrally regulates the pathology of many diseases with an inflammatory basis, including obesity, cardiovascular disease, and cancer.  Although alternatively activated and classically activated macrophage phenotypes can be useful designations, it is apparent that macrophages exist along a phenotypic spectrum and may have the capacity to convert their phenotypes.  Dr. Heller's group is actively engaged in this exciting new area of macrophage immunobiology. New projects include elucidating the links between asthma and obesity and determining how gender and race affect asthma and obesity in humans.  They utilize a variety of techniques, including molecular and cellular biology, biochemistry, mouse models, cultured cell lines, and human patient samples to uncover cellular and molecular pathways that will be relevant targets for human clinical benefit.  Dr. Heller maintains active collaborations with faculty members of the Division of Allergy and Clinical Immunology at the Johns Hopkins Asthma and Allergy Center on the Bayview Campus.

Dr. Heller has mentored trainees from high school students to MD/PhDs during her academic career, and she welcomes motivated and interested students.  Many potential projects in the lab can be tailored to fit the interests of students and fellows with a short-term or longer-term time frame.  Students and fellows will gain hands-on experience in a variety of cutting-edge techniques by working on their own project and will be able to observe and/or participate in other ongoing research projects in the lab.  Students and fellows will have the opportunity to interact with Dr. Heller on a daily basis, often at the bench.

Laboratory members

Lab Manager
Jessie X. Fang, MS

Postdoctoral Fellow
Nagaraj Gowda, PhD

  • We welcome inquiries from interested postdoctoral fellows, graduate students, and undergraduates about research opportunities in the lab.

Selected Publications

  1. Heller NM, Gwinn WM, Donnelly RP, Constant SL, Keegan AD. IL-4 Engagement of the type I IL-4 receptor complex enhances mouse eosinophil migration to eotaxin-1 in vitro. PLoS One 7(6): e39673, 2012.
  2. Ford AQ, Heller NM, Stephenson L, Boothby MR, Keegan AD. An atopy-associated polymorphism in the ectodomain of the IL-4R(alpha) chain (V50) regulates the persistence of STAT6 phosphorylation.  J Immunol  183(3):1607-1616, 2009.
    • This paper was highlighted for its clinical relevance on (Allergy/Immunology section).
  3. Heller NM, Qi X, Junttila IS, Shirey KA, Vogel SN, Paul WE, Keegan AD. Type I IL-4Rs selectively activate IRS-2 to induce target gene expression in macrophages.  Sci Signaling  1(51): ra17, 2008.
    • This paper was the subject of a Perspective Review in the same issue:  
      Wills-Karp M, Finkelman FD. Untangling the complex web of IL-4- and IL-13-mediated signaling pathways.  Sci Signal. 1: pe55, 2008.
    • and a Highlight in the Journal of Allergy and Clinical Immunology:
      Rothenberg ME, Nelson HS. News Beyond Our Pages.  J Allergy Clin Immunol  123: 517, 2009.
  4. LaPorte SL, Juo ZS, Vaclavikova J, Colf LA, Qi X, Heller NM, Keegan AD, Garcia KC. Molecular and structural basis of cytokine receptor pleiotropy in the interleukin-4/13 system. Cell  132:259-272, 2008.
    • We provide the functional data, i.e. signal transduction analyses, to complement the structural data from the Garcia laboratory.
    • This paper was the basis of the Cover art and a Review in that issue: Zdanov A, Wlodawer A. A new look at cytokine signaling. Cell 132: 179, 2008.
    • and a Research Highlight in Nature Reviews Immunology: Minton K. Allergy and Asthma: What 'drives' IL-4 versus IL-13 signalling? Nat Rev Immunol 8:166, 2008.
  5. Heller NM, Matsukura S, Georas SN, Boothby MR, Rothman PB, Stellato C, Schleimer RP.  Interferon-γ inhibits STAT6 signal transduction and gene expression in human airway epithelial cells.  Am J Respir Cell Mol Biol  31(5):573-582, 2004.
  6. Heller NM, Matsukura S, Georas SN, Boothby MR, Stellato C, Schleimer RP. Assessment of STAT6 as a target of glucocorticoid action in human airway epithelial cells.  Clin Exp Allergy 34(11):1690-1700, 2004.



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