Carla Rothlin, PhD
Research & Publications
Biography
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Research Summary
I co-lead our group with Sourav Ghosh, Associate Professor of Neurology and Pharmacology. We have a long-term interest in how the immune response is calibrated to avoid chronic inflammation, autoimmunity and self-harm. We study mechanisms that set or limit the magnitude of the immune response. We also study mechanisms that signal the temporal shift from a pathogen-defense mode following successful immune defense to resolution and wound repair. One of the current interests in the lab is cell death and its clearance, and how this can function as a signal for specific effector responses during morphogenesis, homeostatic tissue renewal, or resolution and wound repair after damage. We hypothesize that the integration of cell death recognition, environmental signals (including tissue-specific signals) and the identity of the efferocyte (the cell that recognizes dead cells) determines the specificity for removal of dead/damaged cells, renewal of lost cells, or repair and regeneration. We use a variety of approaches including molecular, cell biology, immunology, imaging and genetics and mouse models of development/tissue homeostasis/injury or diseases to address fundamental biological mechanisms.
Current projects:
- Macrophage-stromal interactions during tissue homeostasis and wound repair
- Crosstalk between stromal and immune cells, in the context of cell turnover or injury, during the formation and function of the nervous system
- Innate immune checkpoints and anti-tumor immunity
Extensive Research Description
Immunobiology; Immune Homeostasis; TAM Receptor Tyrosine Kinases
Coauthors
Research Interests
Inflammation
Selected Publications
- Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells.Bosurgi L, Cao YG, Cabeza-Cabrerizo M, Tucci A, Hughes LD, Kong Y, Weinstein JS, Licona-Limon P, Schmid ET, Pelorosso F, Gagliani N, Craft JE, Flavell RA, Ghosh S, Rothlin CV. Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. Science (New York, N.Y.) 2017, 356: 1072-1076. PMID: 28495875, PMCID: PMC5556699, DOI: 10.1126/science.aai8132.
- AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity.Schmid ET, Pang IK, Carrera Silva EA, Bosurgi L, Miner JJ, Diamond MS, Iwasaki A, Rothlin CV. AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity. ELife 2016, 5 PMID: 27350258, PMCID: PMC4924996, DOI: 10.7554/eLife.12414.
- The TAM family receptor tyrosine kinase TYRO3 is a negative regulator of type 2 immunity.Chan PY, Carrera Silva EA, De Kouchkovsky D, Joannas LD, Hao L, Hu D, Huntsman S, Eng C, Licona-Limón P, Weinstein JS, Herbert DR, Craft JE, Flavell RA, Repetto S, Correale J, Burchard EG, Torgerson DG, Ghosh S, Rothlin CV. The TAM family receptor tyrosine kinase TYRO3 is a negative regulator of type 2 immunity. Science (New York, N.Y.) 2016, 352: 99-103. PMID: 27034374, PMCID: PMC4935984, DOI: 10.1126/science.aaf1358.
- TAM receptor signaling in immune homeostasis.Rothlin CV, Carrera-Silva EA, Bosurgi L, Ghosh S. TAM receptor signaling in immune homeostasis. Annual Review Of Immunology 2015, 33: 355-91. PMID: 25594431, PMCID: PMC4491918, DOI: 10.1146/annurev-immunol-032414-112103.
- Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma.Kusne Y, Carrera-Silva EA, Perry AS, Rushing EJ, Mandell EK, Dietrich JD, Errasti AE, Gibbs D, Berens ME, Loftus JC, Hulme C, Yang W, Lu Z, Aldape K, Sanai N, Rothlin CV, Ghosh S. Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma. Science Signaling 2014, 7: ra75. PMID: 25118327, PMCID: PMC4486020, DOI: 10.1126/scisignal.2005196.