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• W2588897494 abstract "Mannan binding lectin (MBL), initially reported to activate the complement pathway, is also known to be involved in the pathogenesis of autoimmune diseases. We report a thus far unknown function of MBL as a suppressor of T-cell activation. MBL markedly inhibited T-cell proliferation induced by anti-CD3 and anti-CD28 antibodies. Moreover, the presence of MBL during T-cell priming interfered with proximal T-cell receptor signaling by decreasing phosphorylation of Lck, ZAP-70, and LAT. MBL bound to T cells through interaction between the collagen-like region of MBL and calreticulin (CRT) expressed on the T-cell surface. The neutralizing antibody against CRT abrogated MBL-mediated suppression of T-cell proliferation, suggesting that MBL down-modulates T-cell proliferation via cell surface CRT. We further demonstrated that the feature of MBL-mediated T-cell suppression is shared by other serum collectins (e.g., C1q and collectin 11). The concentrations of MBL correlated negatively with in vivo T-cell activation status in patients with early-stage silicosis. Furthermore, MBL efficiently inhibited activation and proliferation of autoreactive T cells derived from patients with silicosis, indicating that MBL serves as a negative feedback control of the T-cell responses.-Zhao, N., Wu, J., Xiong, S., Zhang, L., Lu, X., Chen, S., Wu, Q., Wang, H., Liu, Y., Chen, Z., Zuo, D. Mannan-binding lectin, a serum collectin, suppresses T-cell proliferation via direct interaction with cell surface calreticulin and inhibition of proximal T-cell receptor signaling." @default.
• W2588897494 created "2017-02-24" @default.
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• W2588897494 date "2017-02-16" @default.
• W2588897494 modified "2023-10-05" @default.
• W2588897494 title "Mannan‐binding lectin, a serum collectin, suppresses T‐cell proliferation<i>via</i>direct interaction with cell surface calreticulin and inhibition of proximal T‐cell receptor signaling" @default.
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• W2588897494 doi "https://doi.org/10.1096/fj.201601200rr" @default.
• W2588897494 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28209773" @default.
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