Postdoctoral Position in Immune Regulation:
The Chatila Lab at the Division of Immunology, Boston Children’s Hospital and Harvard Medical School is recruiting applicants for postdoctoral scholar positions in the areas of regulatory T (Treg) cell biology with a focus autoimmunity and mucosal immune tolerance. Our research aims to elucidate the mechanisms of tolerance breakdown in autoimmune and allergic disorders and the role of the commensal microbiota in shaping immune tolerance and its breakdown in these disorders. The overall aim of these studies is to elucidate tissue-operative regulatory switches that govern immune dysregulatory diseases. The results from these studies will have a profound impact on our understanding of the biology of autoimmune and allergic diseases with the potential to identify new classes of therapeutics for these disorders. Interested candidates are recommended to go through the following articles to obtain insights into the areas that the lab is most interested in.
Relevant publications include:
1. Mechanism of Treg cell reprogramming in autoimmune and allergic 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. Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling. Nat Immunol. 2015 Nov;16(11):1162-73.
c. Charbonnier LM et al. Functional reprogramming of regulatory T cells in the absence of Foxp3. Nat Immunol. 2019 Sep;20(9):1208-1219.
2. Treg cell molecular switches that control tissue 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. Harb A et al. A regulatory T cell Notch4-GDF15 axis licenses tissue inflammation in asthma. Nat Immunol. 2020 Nov;21(11):1359-1370.
c., Harb A, Benamar M et al. Notch4 signaling limits regulatory T cell mediated tissue repair and promotes severe lung inflammation in viral infections. Immunity 2021 (in press).
3. Role of the Treg cells and the microbiota in mucosal tolerance.
a. Wang, S. et al. MyD88 Adaptor-Dependent Microbial Sensing by Regulatory T Cells Promotes Mucosal Tolerance and Enforces Commensalism. Immunity. 2015 Aug 18;43(2):289-303.
b. 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.
c. Turner JA et al. Regulatory T Cell-Derived TGF-β1 Controls Multiple Checkpoints Governing Allergy and Autoimmunity. Immunity. 2020 Dec 15;53(6):1202-1214.
d. Stephen-Victor E, et al. Dietary and Microbial Determinants in Food Allergy. Immunity. 2020 Aug 18;53(2):277-289.
The postdoctoral candidates must have PhD in Immunology or related field, and a track record of productivity with peer-reviewed publications. The ideal candidate should have a strong background in Treg cell biology, autoimmunity and/or mucosal immunology. A good knowledge of molecular biology and bioinformatics is highly desirable. The lab comprises of 10 members including Instructors, postdocs, and research assistants and hence the candidate must be motivated, have a propensity to work individually and along with a team. Please send a motivation letter explaining your interest in this job advertisement, CV and the names of three references to firstname.lastname@example.org. Salary will follow NIH guidelines commensurate with training and experience. Boston Children’s Hospital, Harvard Medical School is an Affirmative Action/Equal Opportunity Employer.
Tagged as: Life Sciences
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