A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
LINC01871 is exclusively expressed in T and NK cells and is highly induced upon CD4+ T cell activation
Tekijät: Kalim, 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
Kustantaja: Cell Press
Julkaisuvuosi: 2025
Lehti: iScience
Artikkelin numero: 113779
Vuosikerta: 28
Numero: 11
eISSN: 2589-0042
DOI: https://doi.org/10.1016/j.isci.2025.113779
Julkaisun avoimuus kirjaamishetkellä: Avoimesti saatavilla
Julkaisukanavan avoimuus : Kokonaan avoin julkaisukanava
Verkko-osoite: https://doi.org/10.1016/j.isci.2025.113779
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/505586490
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.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
Julkaisussa olevat rahoitustiedot:
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.
