The Chatila Lab at the Division of Immunology, Boston Children’s Hospital and Harvard Medical School, is recruiting two applicants for postdoctoral scholar positions in the areas of mucosal Immune tolerance, with a focus on the role of the regulatory T (Treg) cells and the microbiota in food allergy and asthma. Our research aims to elucidate the mechanisms of tolerance breakdown in allergic disorders and the role of the commensals in monitoring immunity to allergic diseases. The eventual goal of our studies is to identify and describe a framework of tissue operative regulatory switches that govern allergic disorders. Their outcome will deepen our understanding of the biology of allergic diseases with the potential to develop novel therapeutics for allergic disorders. Interested candidates are recommended to consult our following publications to obtain insights on the areas that the lab is most interested in.
1. Role of the gut microbiota and metabolites in regulating Food allergy.
a. Abdel-Gadir A et al. Microbiota therapy acts via a regulatory T cell MyD88/RORγt pathway to suppress food allergy. Nat Med. 2019 Jul;25(7):1164-1174.
b. Noval Rivas M et al. A microbiota signature associated with experimental food allergy promotes allergic sensitization and anaphylaxis. J Allergy Clin Immunol. 2013 Jan;131(1):201-12.
c. Crestani E et al. Untargeted metabolomic profiling identifies disease-specific signatures in food allergy and asthma. J Allergy Clin Immunol. 2019 Oct 25. pii: S0091-6749(19)31402-2.
2. Mechanism of Treg cell reprogramming in allergic and autoimmune diseases.
a. Noval Rivas M et al. Regulatory T cell reprogramming toward a Th2-cell-like lineage impairs oral tolerance and promotes food allergy.Immunity. 2015 Mar 17;42(3):512-23.
b. Charbonnier LM et al. Functional reprogramming of regulatory T cells in the absence of Foxp3. Nat Immunol. 2019 Sep;20(9):1208-1219.
c. Charbonnier LM et al. Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling. Nat Immunol. 2015 Nov;16(11):1162-73.
3. Molecular switches that regulate allergic airway inflammation.
a. Massoud A et al. An asthma-associated IL4R variant exacerbates airway inflammation by promoting conversion of regulatory T cells to TH17-like cells. Nat Med. 2016 Sep;22(9):1013-22.
b. Xia M et al. A Jagged 1-Notch 4 molecular switch mediates airway inflammation induced by ultrafine particles. J Allergy Clin Immunol. 2018 Oct;142(4):1243-1256.e17.
The postdoctoral candidates must have PhD in Immunology or related field, a track record of productivity with peer-reviewed publications. The ideal candidate should have a strong background in Treg cell biology, mucosal immunology and/or microbiota studies. Candidates must be motivated, have a propensity to work independently and also as part of the lab team. Please send a motivation letter explaining your interest in this job advertisement, CV and the names of at least 3 references to email@example.com. Salary will follow NIH guidelines commensurate with training and experience. Boston Children’s Hospital, Harvard Medical School is an Affirmative Action/Equal Opportunity Employer.