A1 Refereed original research article in a scientific journal

LINC01871 is exclusively expressed in T and NK cells and is highly induced upon CD4+ T cell activation




AuthorsKalim, Ubaid Ullah; Shetty, Ankitha; Ranade, Amogh; Rundquist, Olof; Starskaia, Inna; Batkulwar, Kedar; Välikangas, Tommi; Sousa, António G. G.; Hurme, Antti; Kumpulainen, Venla; Viitala, Miro; Kosola, Sakari; Junttila, Sini; Rasool, Omid; Elo, Laura L.; Galande, Sanjeev; Lahesmaa, Riitta

PublisherCell Press

Publication year2025

Journal: iScience

Article number113779

Volume28

Issue11

eISSN2589-0042

DOIhttps://doi.org/10.1016/j.isci.2025.113779

Publication's open availability at the time of reportingOpen Access

Publication channel's open availability Open Access publication channel

Web address https://doi.org/10.1016/j.isci.2025.113779

Self-archived copy’s web addresshttps://research.utu.fi/converis/portal/detail/Publication/505586490


Abstract
Long intergenic noncoding RNAs (lincRNAs) regulate biological processes in health and disease. Recent findings highlight the importance of lincRNAs in regulating T cell development and function. Here, we identified a lincRNA, LINC01871, which is highly induced upon CD4+ T cell activation and is predominantly located in the cytoplasm. The anti-inflammatory cytokine TGF-β was found to suppress its expression. Silencing LINC01871 led to a modest decrease in IL-2 secretion. Notably, LINC01871 expression was highly specific to NK cells and T cells in several cross-tissue single cell RNA-seq atlases. These data suggest that LINC01871 is specifically expressed in T and NK cells and may contribute to T cell-mediated immunity in humans.

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Funding information in the publication
R.L. is supported by Research Council of Finland grants 250114, 292335, 294337, 292482, 319280, 329277, 331793, 335435, and 31444; Breakthrough T1D Foundation grant; the Novo Nordisk Foundation grant NNF19OC0057218; Jane and Aatos Erkko Foundation grant; and the Finnish Cancer Foundation grant. L.L.E. is supported by European Research Council ERC 677943, European Union’s Horizon 2020 research and innovation program 955321; and Research Council of Finland grants 310561, 314443, 329278, 335434, 335611, and 341342. R.L. and L.L.E. were supported by the Sigrid Jusélius Foundation, Turku Graduate School University of Turku, Åbo Akademi University InFLAMES Flagship Program of the Research Council of Finland 337530, Biocenter Finland, and ELIXIR Finland. AGGS was supported by the European Union’s Horizon 2020 Research and Innovation Program under the Marie Skłodowska-Curie grant agreement no.: 955321. O Rundquist. was supported by the Finnish Cultural Foundation and the Sakari Alhopuro Foundation grants, K.B. was supported by the Finnish Cultural Foundation grant.


Last updated on 2025-28-11 at 15:51