Browsing by Author "Wei, Jun"

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    Circulating Antibodies to Linear Peptide Antigens Derived from ANXA1 and FOXP3 in Lung Cancer
    (IIAR, 2017-06) Wang, Weili; Zhong, Wen; Chen, Cairen; Meng, Qingyong; Wei, Jun; Radiation Oncology, School of Medicine
    Background: Our previous studies revealed that concentrations of circulating antibodies to annexin A1 (ANXA1) and forkhead-box P3 (FOXP3) increased significantly in patients with non-small cell lung cancer (NSCLC). This study was thus undertaken to replicate our initial findings with different sample sets. Patients and Methods: Antibodies were tested in 108 patients with NSCLC and 216 controls, who were divided into the discovery (49 vs. 108) and validation (60 vs. 108) group based on the time of enrolment. Results: Analysis of the discovery group showed a significant increase in circulating anti-ANXA1 IgG levels in the patient group compared with the control group (p=0.005) but the validation group simply exhibited a trend toward an increase in IgG levels in NSCLC (p=0.238), generating a combined p-value of 0.009. Conclusion: The findings of this study support the notion that circulating IgG antibodies to ANXA1 could be used as a biomarker for early diagnosis of NSCLC but failed to replicate such findings for FOXP3.
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    PTEN directs developmental and metabolic signaling for innate-like T cell fate and tissue homeostasis
    (Springer Nature, 2022) Blanco, Daniel Bastardo; Chapman, Nicole M.; Raynor, Jana L.; Xu, Chengxian; Su, Wei; Anil, K. C.; Li, Wei; Lim, Seon Ah; Schattgen, Stefan; Shi, Hao; Risch, Isabel; Sun, Yu; Dhungana, Yogesh; Kim, Yunjung; Wei, Jun; Rankin, Sherri; Neale, Geoffrey; Thomas, Paul G.; Yang, Kai; Chi, Hongbo; Pediatrics, School of Medicine
    Phosphatase and tensin homologue (PTEN) is frequently mutated in human cancer, but its roles in lymphopoiesis and tissue homeostasis remain poorly defined. Here we show that PTEN orchestrates a two-step developmental process linking antigen receptor and IL-23-Stat3 signalling to type-17 innate-like T cell generation. Loss of PTEN leads to pronounced accumulation of mature IL-17-producing innate-like T cells in the thymus. IL-23 is essential for their accumulation, and ablation of IL-23 or IL-17 signalling rectifies the reduced survival of female PTEN-haploinsufficient mice that model human patients with PTEN mutations. Single-cell transcriptome and network analyses revealed the dynamic regulation of PTEN, mTOR and metabolic activities that accompanied type-17 cell programming. Furthermore, deletion of mTORC1 or mTORC2 blocks PTEN loss-driven type-17 cell accumulation, and this is further shaped by the Foxo1 and Stat3 pathways. Collectively, our study establishes developmental and metabolic signalling networks underpinning type-17 cell fate decisions and their functional effects at coordinating PTEN-dependent tissue homeostasis.