Rachel A Gottschalk, PhD
- Post-doctoral Fellowship, Laboratory of Systems Biology, NIAID, NIH
- PhD in Immunology, Weill Cornell Graduate School of Medical Sciences, 2012
- BS in Biology, Emory University, 2005
Assistant Professor, Department of Immunology
Member, Graduate Program in Microbiology and Immunology (PMI)
Our lab uses quantitative approaches to understand how cells process stimuli to determine the appropriate functional response. Identifying the receptors, kinases, and transcription factors that make up signaling pathways is necessary but not sufficient to predict how a cell will respond. Context-dependent factors, such as tissue-specific stimuli, age, or genetic traits, can cause small variations in signaling components. These changes may tune the sensitivity of cells to stimuli, setting the threshold for a functional response and influencing susceptibility to disease
The major focus of our lab is understanding context-specific macrophage signaling and function. One such context is the tissue-specific tuning of macrophage signaling at barrier sites, where macrophages face ongoing exposure to the microbiota. These efforts involve modeling how lung-specific homeostatic cytokines impact regulation of macrophage signaling and gene expression, and investigation of novel signaling regulators that are highly expressed in the lung, but not other tissues. Current projects also include interrogating the influence of aging on monocyte and macrophage signaling sensitivity and response dynamics. Specifically, we are investigating whether monocytes from young and old humans or mice have distinct potential for functional polarization, in vitro and in mouse models of inflammation and resolution. We hope our efforts will bring us closer to predicting inflammatory response regulation based on context-specific gene expression, informing tissue-specific and age-specific therapeutic strategies.
Gottschalk RA*#, Dorrington MG*, Dutta B, Krauss KS, Martins AJ, Uderhardt S, Chan W, Tsang JS, Torabi-Parizi P, Fraser ID and Germain RN.# 2019. IFN-mediated negative feedback supports bacteria class-specific macrophage inflammatory responses. eLIFE. 8: e46836. *co-first authors, #co-corresponding authors
Oh KS*, Gottschalk RA*#, Lounsbury NW*, Sun J, Dorrington MG, Baek S, Sun G, Wang Z, Krauss KS, Milner JD, Dutta B, Hager GL, Sung MH and Fraser ID.# 2017. Dual roles for Ikaros in regulation of macrophage chromatin state and inflammatory gene expression. J. Immunol. 201: 757-771. *co-first authors, #co-corresponding authors
Oh KS, Patel H, Gottschalk RA, Lee WS, Baek S, Fraser ID, Hager GL and Sung MH. 2017. Anti-inflammatory chromatinscape suggests alternative mechanisms of glucocorticoid receptor action. Immunity. 47: 298-309.
Martins AJ, Narayanan M, Prüstel T, Fixsen B, Park K, Gottschalk RA, Lu Y, Pfannkoch C, Lau WW, Wendelsdorf KV and Tsang JS. 2017. Environment tunes propagation of cell-to-cell variation in the human macrophage gene network. Cell Systems. 4: 379-392.
Gottschalk RA*, Martins AJ, Angermann BR, Dutta B, Ng CE, Uderhardt S, Tsang JS, Fraser ID, Meier-Schellersheim M and Germain RN.* 2016. Distinct NF-kB and MAPK activation thresholds uncouple steady-state microbe sensing from anti-pathogen inflammatory responses. Cell Systems. 2: 378-90. *co-corresponding authors
- Macrophage signaling
- Quantitative control of inflammation
- Tissue-specific macrophage function
- Computational and systems biology