Rachel A. Gottschalk, Ph.D.

  • Assistant Professor
  • Department of Immunology

Education & Training

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

Research Interest Summary

Our lab uses quantitative approaches to understand how macrophages process stimuli to determine the appropriate immune function.

Research Categories

Research Interests

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.

Representative Publications

Cheemalavagu N, Shoger KE, Cao YM, 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

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

Myers S.A., Gottschalk R.A. Mechanisms encoding STAT functional diversity for context-specific inflammatory responses. Curr. Opin. Immunol. Feb;74:150-155, 2022

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

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

Oh K.S.*, Gottschalk R.A.*#, Lounsbury N.W.*, Sun J., Dorrington M.G., Baek S., Sun G., Wang Z., Krauss K.S., Milner J.D., Dutta B., Hager G.L., Sung M.H., Fraser I.D.# Dual roles for Ikaros in regulation of macrophage chromatin state and inflammatory gene expression. J. Immunol. 201(2):757-771, 2018 *co-first authors, #co-corresponding authors

Oh K.S., Patel H., Gottschalk R.A., Lee W.S., Baek S., Fraser I.D., Hager G.L., Sung M.H. Anti-inflammatory chromatinscape suggests alternative mechanisms of glucocorticoid receptor action. Immunity. 47(2):298-309, 2017

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

Gottschalk R.A., Hathorn M.M., Beuneu H., Corse E., Dustin M.L., Altan-Bonnet G., Allison J.P. Distinct influences of peptide-MHC quality and quantity on in vivo T cell responses. Proc Natl Acad Sci. 109(3): 881-886, 2012

Gottschalk R.A., Corse E., Allison J.P. TCR ligand density and affinity determine peripheral induction of Foxp3 in vivo. J Exp Med. 207(8): 1701-11, 2010

Full List of Publications