| Literature DB >> 33878293 |
Teresa Sadras1, Mickaël Martin2, Kohei Kume3, Mark E Robinson3, Supraja Saravanakumar4, Gal Lenz5, Zhengshan Chen4, Joo Y Song6, Tanya Siddiqi7, Laura Oksa8, Anne Marie Knapp9, Jevon Cutler10, Kadriye Nehir Cosgun3, Lars Klemm3, Veronika Ecker11, Janet Winchester4, Dana Ghergus12, Pauline Soulas-Sprauel2, Friedemann Kiefer13, Nora Heisterkamp4, Akhilesh Pandey10, Vu Ngo4, Lili Wang4, Hassan Jumaa14, Maike Buchner15, Jürgen Ruland15, Wing-Chung Chan6, Eric Meffre16, Thierry Martin17, Markus Müschen18.
Abstract
Even though SYK and ZAP70 kinases share high sequence homology and serve analogous functions, their expression in B and T cells is strictly segregated throughout evolution. Here, we identified aberrant ZAP70 expression as a common feature in a broad range of B cell malignancies. We validated SYK as the kinase that sets the thresholds for negative selection of autoreactive and premalignant clones. When aberrantly expressed in B cells, ZAP70 competes with SYK at the BCR signalosome and redirects SYK from negative selection to tonic PI3K signaling, thereby promoting B cell survival. In genetic mouse models for B-ALL and B-CLL, conditional expression of Zap70 accelerated disease onset, while genetic deletion impaired malignant transformation. Inducible activation of Zap70 during B cell development compromised negative selection of autoreactive B cells, resulting in pervasive autoantibody production. Strict segregation of the two kinases is critical for normal B cell selection and represents a central safeguard against the development of autoimmune disease and B cell malignancies.Entities:
Keywords: Anergy; B cell selection; Kinases; Leukemia; NFAT; Tolerance
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Year: 2021 PMID: 33878293 PMCID: PMC8239336 DOI: 10.1016/j.molcel.2021.03.043
Source DB: PubMed Journal: Mol Cell ISSN: 1097-2765 Impact factor: 17.970