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Nicola
M.
Heller
,
PhD

Associate Professor
Nicola Heller

Departmental Affiliations

School of Medicine
Primary

Contact Info

720 Rutland Avenue, Ross 367
Baltimore
Maryland
21205
US        
410-614-0083

Research Interests

innate immune system; sex differences; monocytes; macrophages; asthma; lung; IL-4; allergy
Experiences & Accomplishments
Education
PhD
Johns Hopkins School of Medicine
2004
BSc
The University of Bath
1995
Overview
The focus of Dr. Heller’s laboratory is the role of macrophages in promoting and resolving disease, particularly in lung diseases, such as asthma and acute respiratory distress syndrome (ARDS). Improper regulation of macrophage polarization can promote pathogenesis, exemplified by the abundance of M2 or “alternatively activated” macrophages during allergic inflammation of the lung. Dr. Heller is interested in how IL-4 or IL-13 (and other stimuli) induce differentiation of resting macrophages into the M2 phenotype. Her research program focuses on the basic molecular mechanisms of signaling from the biology of the IL-4/IL-13 receptor, signal transduction, and its regulation. Current research projects include determining how sex and sex hormones affect macrophage polarization in asthma. New projects are investigating novel interventions (peptide inhibitors) to block macrophage differentiation in asthma and utilizing nanoparticle-treated monocytes as cellular immunotherapy for ARDS. Her research program utilizes 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 of monocyte-macrophage activation that will be relevant targets for human clinical benefit.
Select Publications
Selected representative publications
  • Keselman A, Fang X, White PB, Heller NM. Estrogen Signaling Contributes to Sex Differences in Macrophage Polarization during Asthma. J Immunol. 2017 Sep 1;199(5):1573-1583. doi: 10.4049/jimmunol.1601975. Epub 2017 Jul 31. PMID: 28760880; PMCID: PMC5576568.
  • Keegan AD, Zamorano J, Keselman A, Heller NM. IL-4 and IL-13 Receptor Signaling From 4PS to Insulin Receptor Substrate 2: There and Back Again, a Historical View. Front Immunol. 2018 May 15;9:1037. doi: 10.3389/fimmu.2018.01037. PMID: 29868002; PMCID: PMC5962649.
  • Becerra-Díaz M, Lerner AD, Yu DH, Thiboutot JP, Liu MC, Yarmus LB, Bose S, Heller NM. Sex differences in M2 polarization, chemokine and IL-4 receptors in monocytes and macrophages from asthmatics. Cell Immunol. 2021 Feb;360:104252. doi: 10.1016/j.cellimm.2020.104252. Epub 2020 Dec 6. PMID: 33450610.
  • D'Alessio FR, Craig JM, Singer BD, Files DC, Mock JR, Garibaldi BT, Fallica J, Tripathi A, Mandke P, Gans JH, Limjunyawong N, Sidhaye VK, Heller NM, Mitzner W, King LS, Aggarwal NR. Enhanced resolution of experimental ARDS through IL-4-mediated lung macrophage reprogramming. Am J Physiol Lung Cell Mol Physiol. 2016 Apr 15;310(8):L733-46. doi: 10.1152/ajplung.00419.2015. Epub 2016 Feb 19. PMID: 26895644; PMCID: PMC4836113.
  • McCormick SM, Gowda N, Fang JX, Heller NM. Suppressor of Cytokine Signaling (SOCS)1 Regulates Interleukin-4 (IL-4)-activated Insulin Receptor Substrate (IRS)-2 Tyrosine Phosphorylation in Monocytes and Macrophages via the Proteasome. J Biol Chem. 2016 Sep 23;291(39):20574-87. doi: 10.1074/jbc.M116.746164. Epub 2016 Aug 9. PMID: 27507812; PMCID: PMC5034051.