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Rachel A. Gottschalk Ph.D.

  • Assistant Professor, Department of Immunology
  • PMI Graduate Faculty

    Education & Training

  • Post-doctoral Fellowship, Laboratory of Systems Biology, NIAID, NIH
  • Ph.D., Immunology, Weill Cornell Graduate School of Medical Sciences, 2012
  • B.S., Biology, Emory University, 2005
Representative Publications

1. Cheemalavagu N, ShogerKE, CaoYM, Michalides BA, Botta SA, Faeder JR, Gottschalk RA. Predicting gene level sensitivity to JAK-STAT signaling perturbation using a mechanistic-to-machine learning framework. Cell Syst. Jan 17;15(1):37-48, 2024/p>

2.     Gottschalk R.A. Signaling is the pathway to macrophage function. Trends Immunol. May 29;S1471-4906(23)00080-7, 2023

3.     Shoger K.E., Cheemalavagu N., Cao Y.M., Michalides B.A., Chaudhri V.K., Cohen J.A., Singh H., GottschalkR.A. CISH attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function. Sci Signal. 14(698):eabe5137, 2021

4.     Gottschalk R.A.*#, Dorrington M.G.*, Dutta B., Krauss K.S., Martins A.J., Uderhardt S., Chan W., Tsang J.S., Torabi-Parizi P., Fraser I.D., Germain R.N.#. IFN-mediated negative feedback supports bacteria class-specific macrophage inflammatory responses. eLIFE. 2019;8:e46836, 2019

*co-first authors, #co-corresponding authors

5.     Gottschalk R.A.#, Martins A.J., Angermann B.R., Dutta B., Ng C.E., Uderhardt S., Tsang J.S., Fraser I.D., Meier-Schellersheim M., Germain R.N.# Distinct NF-kB and MAPK activation thresholds uncouple steady-state microbe sensing from anti-pathogen inflammatory responses. Cell Syst. 2(6): 378-90, 2016

#co-corresponding authors

Complete list of publications

Research Interests
  • Macrophage signaling
  • Quantitative control of inflammation
  • Tissue-specific macrophage function
  • Computational and systems biology

Understanding how extracellular cues are linked to gene expression is a fundamental challenge in biology, and more specifically, innate immune signal integration is central to understanding healthy versus aberrant regulation of inflammation. My laboratory uses quantitative approaches to address these problems, with major projects including (1) computational modeling of signaling-to-transcription in macrophages, (2) interrogating tissue-specific macrophage signaling, and (3) dissecting molecular determinants of monocyte and macrophage inflammatory function. We use experimental approaches, together with both data-driven and mechanistic modeling to integrate transcription factor activity, phosphorylation, and transcriptomic data to explore signaling mechanisms that shape stimulus-specific macrophage function. These efforts will yield insights into dysregulation of signaling and inflammation, while informing therapeutic strategies.