Interferon Receptor Chain Deficiency in Murine Friend Erythroleukemia Cell Clone Resistant to Type I or Type I and II Interferons

Interferon (IFN)-resistant cell clones 3Cl8 and 3γR8, isolated from wild-type Friend erythroleukemia cells 745A were characterized to identify the resistance defect. The 3Cl8 cell clone is resistant to type I IFNs and sensitive to type II IFN, whereas 3γR8, derived from 3Cl8, is resistant to both type I and II IFNs. Here, we report that no activation of the JAK-STAT pathway is detected after IFN treatment of resistant cells. Interestingly, the absence of major transcripts of the IFNAR2 receptor chain has been observed in type I IFN-resistant cells, and a point mutation relative to the IFNGR2 receptor chain (β chain) has been identified in type II IFN-resistant cells, inducing a frameshift leading to premature termination of translation. In addition, we have identified a new polymorphism of the murine IFNAR1 chain and possibly the presence of a murine IFNAR2b transmembrane, non-transducing chain in 745A cells, similar to that observed in humans and differing from previous reports on other murine systems.

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Journal
International Journal of Molecular Sciences
Published
2026-06-30
DOI
https://doi.org/10.3390/ijms27135908
Primary Topic
Cytokine Signaling Pathways and Interactions
Type
article
Field-Weighted Citation Impact
0.00

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article

Interferon Receptor Chain Deficiency in Murine Friend Erythroleukemia Cell Clone Resistant to Type I or Type I and II Interferons

Zulema Percario, Giorgio Mangino, Gabriele Vaccari, Arianna Raponi et al.
International Journal of Molecular Sciences
Cytokine Signaling Pathways and Interactions
article

Interferon Receptor Chain Deficiency in Murine Friend Erythroleukemia Cell Clone Resistant to Type I or Type I and II Interferons

Zulema Percario, Giorgio Mangino, Gabriele Vaccari, Arianna Raponi, Elisabetta Affabris, Emiliano Fratini, Flavia Giannessi, Gianna Fiorucci, Manuela Cervelli, G. Romeo
article en

Abstract

Interferon (IFN)-resistant cell clones 3Cl8 and 3γR8, isolated from wild-type Friend erythroleukemia cells 745A were characterized to identify the resistance defect. The 3Cl8 cell clone is resistant to type I IFNs and sensitive to type II IFN, whereas 3γR8, derived from 3Cl8, is resistant to both type I and II IFNs. Here, we report that no activation of the JAK-STAT pathway is detected after IFN treatment of resistant cells. Interestingly, the absence of major transcripts of the IFNAR2 receptor chain has been observed in type I IFN-resistant cells, and a point mutation relative to the IFNGR2 receptor chain (β chain) has been identified in type II IFN-resistant cells, inducing a frameshift leading to premature termination of translation. In addition, we have identified a new polymorphism of the murine IFNAR1 chain and possibly the presence of a murine IFNAR2b transmembrane, non-transducing chain in 745A cells, similar to that observed in humans and differing from previous reports on other murine systems.

International Journal of Molecular SciencesVol. 27(13)
Roma Tre University (IT), Istituto Superiore di Sanità (IT), Institute of Molecular Biology and Pathology (IT), National Agency for New Technologies Energy and Sustainable Economic Development (GB), Sapienza University of Rome (IT)
Università degli Studi Roma Tre, Dipartimenti di Eccellenza
Good health and well-being
Openalex Percentile: Top 9%
Cytokine Signaling Pathways and Interactions
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