PI
Research Group
Mohamed Elsherif Badr
sherif.badr(at)cimrbj.ac.cn
Assistant Investigator
T Cell Biology, Immune Tolerance, Autoimmunity
B.S. in Pharmaceutical Sciences, Cairo University, Egypt
M.S. in Medical Sciences, Kanazawa University, Japan
Ph.D. in Biomedical Science, Tokyo Medical and Dental University, Japan
Work Experience
2025–Present
Assistant Investigator, Chinese Institute for Immunology, Chinese Institutes for Medical Research, Beijing, China
2024–2025
Staff Scientist, National Cancer Institute (NCI)/National Institutes of Health (NIH), USA
2016–2024
Research Fellow, National Cancer Institute (NCI)/National Institutes of Health (NIH), USA
2015–2016
Postdoctoral Fellow, RIkagaku KENkyusho/Institute of Physical and Chemical Research (RIKEN), Japan
Research Interests
Research Interests

The Badr Laboratory at the Chinese Institutes for Medical Research (CIMR) is interested in understanding the fundamental mechanisms that maintain immune tolerance and prevent harmful self-reactivity. The lab's research focuses on autoreactive T cells and the molecular, cellular, and developmental pathways that determine their fate in health and disease. By integrating basic immunology with translational approaches, the lab aims to develop new therapeutic strategies for autoimmune diseases and cancer.

The lab's current research interests include:

1. Mechanisms regulating autoreactive T cell development, selection, and tolerance during thymic development and in peripheral tissues.
2. The role of autoreactive T cells in the pathogenesis of autoimmune diseases, including multiple sclerosis, type 1 diabetes, and autoimmune hepatitis.
3. How tolerized autoreactive T cells contribute to tumor immune evasion and whether these cells can be reprogrammed for cancer immunotherapy.
4. Translational studies bridging mouse models and human disease through the use of tissue organoids, single-cell transcriptomics, and TCR sequencing to identify clinically relevant therapeutic targets.
Major Contributions

1. Discovery of Clonal Eviction as a novel mechanism for autoreactive T cell tolerance — revealed that autoreactive CD8 T cells are not deleted in the thymus but instead prematurely exported as immature precursors that later differentiate into self-tolerant regulatory-like cells, redefining the classical view of central tolerance (Science, 2023).

2. Pathways controlling effector and helper T cell programming — identified CRTAM as a key driver of CD4⁺ cytotoxic T cell lineage commitment and uncovered nucleic acid sensing as a trigger for Th2 differentiation, providing new insights into how signals shape T cell fate (J Exp Med, 2016; Nat Commun, 2014).

3. Role of chemokine signaling in central tolerance — demonstrated how Sirpα⁺ dendritic cells and the chemokine receptor CCR2 orchestrate thymic tolerance and facilitate tumor immune evasion, highlighting the intersection of central tolerance and cancer biology (PLoS One, 2012).

Representative Publications     *:Co-first author; #:Co-corresponding author
Representative Publications *:Co-first author; #:Co-corresponding author

Badr M#, Zhang Z, Tai X, Singer A#. CD8 T cell tolerance results from eviction of immature autoreactive cells from the thymus. Science, 2023, 382: 534–541. DOI: 10.1126/science.adh4124

Tai X, Indart A, Rojano M, Guo J, Apenes N, Kadakia T, Craveiro M, Alag A, Etzensperger R, Badr M, Zhang F, Zhang Z, Mu J, Guinter T, Crossman A, Granger L, Sharrow S, Zhou X, Singer A. How autoreactive thymocytes differentiate into regulatory versus effector CD4 T cells after avoiding clonal deletion. Nat Immunol, 2023, 24: 637–651. DOI: 10.1038/s41590-023-01469-2

Badr M, Hata K, Furuhata M, Toyota H, Yokosuka T. The multifaceted role of PD-1 in health and disease. In: Miyasaka M, Takatsu K (eds). Chronic Inflammation. Springer, Tokyo. 2016: 441–457.

Takeuchi A, Badr M, Miyauchi K, Ishihara C, Onishi R, Guo Z, Sasaki Y, Ike H, Takumi A, Tsuji N, Murakami Y, Katakai T, Kubo M, Saito T. CRTAM determines the CD4⁺ cytotoxic T lymphocyte lineageJ Exp Med, 2016, 213: 123–138. DOI: 10.1084/jem.20150519

Imanishi T, Ishihara C, Badr M, Hashimoto-Tane A, Kimura Y, Kawai T, Takeuchi O, Ishii KJ, Taniguchi S, Noda T, Hirano H, Brombacher F, Barber GN, Akira S, Saito T. Nucleic acid sensing by T cells initiates Th2 cell differentiationNat Commun, 2014, 5: 3566. DOI: 10.1038/ncomms4566

Baba T, Badr M, Tomaru U, Ishizu A, Mukaida N. Novel process of intrathymic tumor immune tolerance through CCR2-mediated recruitment of Sirpα⁺ dendritic cells: a murine modelPLoS One, 2012, 7: e41154. DOI: 10.1371/journal.pone.0041154