| Literature DB >> 32078336 |
Fei Han1, Emilia R Dellacecca1, Levi W Barse2, Cormac Cosgrove1, Steven W Henning1, Christian M Ankney3, Dinesh Jaishankar1, Alexander Yemelyanov4, Vera P Krymskaya5, Daniel F Dilling6, I Caroline Le Poole1,7.
Abstract
Patients with lymphangioleiomyomatosis (LAM) develop pulmonary cysts associated with neoplastic, smooth muscle-like cells that feature neuroendocrine cell markers. The disease preferentially affects premenopausal women. Existing therapeutics do not cure LAM. As gp100 is a diagnostic marker expressed by LAM lesions, we proposed to target this immunogenic glycoprotein using TCR transgenic T cells. To reproduce the genetic mutations underlying LAM, we cultured Tsc2-/- kidney tumor cells from aged Tsc2 heterozygous mice and generated a stable gp100-expressing cell line by lentiviral transduction. T cells were isolated from major histocompatibility complex-matched TCR transgenic pmel-1 mice to measure cytotoxicity in vitro, and 80% cytotoxicity was observed within 48 hours. Antigen-specific cytotoxicity was likewise observed using pmel-1 TCR-transduced mouse T cells, suggesting that transgenic T cells may likewise be useful to treat LAM in vivo. On intravenous injection, slow-growing gp100+ LAM-like cells formed lung nodules that were readily detectable in severe combined immunodeficient/beige mice. Adoptive transfer of gp100-reactive but not wild-type T cells into mice significantly shrunk established lung tumors, even in the absence of anti-PD-1 therapy. These results demonstrate the treatment potential of adoptively transferred T cells to eliminate pulmonary lesions in LAM.Entities:
Keywords: T cell receptor; adoptive T cell transfer; gp100; lymphangioleiomyomatosis
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Year: 2020 PMID: 32078336 PMCID: PMC7710336 DOI: 10.1165/rcmb.2019-0117OC
Source DB: PubMed Journal: Am J Respir Cell Mol Biol ISSN: 1044-1549 Impact factor: 6.914