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J Immunol
. 2024 Mar 4:ji2300270.
doi: 10.4049/jimmunol.2300270. Online ahead of print. PRMT5 Promotes T follicular helper Cell Differentiation and Germinal Center Responses during Influenza Virus Infection
Kaitlin A Read 1 2 , Stephanie A Amici 3 , Sadaf Farsi 3 , Madeline Cutcliffe 4 , Bella Lee 1 2 5 , Chan-Wang Jerry Lio 1 6 , Hsin-Jung Joyce Wu 1 4 6 , Mireia Guerau-de-Arellano 1 4 7 , Kenneth J Oestreich 1 6
Affiliations
Protein arginine methyltransferases (PRMTs) modify diverse protein targets and regulate numerous cellular processes; yet, their contributions to individual effector T cell responses during infections are incompletely understood. In this study, we identify PRMT5 as a critical regulator of CD4+ T follicular helper cell (Tfh) responses during influenza virus infection in mice. Conditional PRMT5 deletion in murine T cells results in an almost complete ablation of both Tfh and T follicular regulatory populations and, consequently, reduced B cell activation and influenza-specific Ab production. Supporting a potential mechanism, we observe elevated surface expression of IL-2Rα on non-T regulatory effector PRMT5-deficient T cells. Notably, IL-2 signaling is known to negatively impact Tfh differentiation. Collectively, our findings identify PRMT5 as a prominent regulator of Tfh programming, with potential causal links to IL-2 signaling.
. 2024 Mar 4:ji2300270.
doi: 10.4049/jimmunol.2300270. Online ahead of print. PRMT5 Promotes T follicular helper Cell Differentiation and Germinal Center Responses during Influenza Virus Infection
Kaitlin A Read 1 2 , Stephanie A Amici 3 , Sadaf Farsi 3 , Madeline Cutcliffe 4 , Bella Lee 1 2 5 , Chan-Wang Jerry Lio 1 6 , Hsin-Jung Joyce Wu 1 4 6 , Mireia Guerau-de-Arellano 1 4 7 , Kenneth J Oestreich 1 6
Affiliations
- PMID: 38436421
- DOI: 10.4049/jimmunol.2300270
Protein arginine methyltransferases (PRMTs) modify diverse protein targets and regulate numerous cellular processes; yet, their contributions to individual effector T cell responses during infections are incompletely understood. In this study, we identify PRMT5 as a critical regulator of CD4+ T follicular helper cell (Tfh) responses during influenza virus infection in mice. Conditional PRMT5 deletion in murine T cells results in an almost complete ablation of both Tfh and T follicular regulatory populations and, consequently, reduced B cell activation and influenza-specific Ab production. Supporting a potential mechanism, we observe elevated surface expression of IL-2Rα on non-T regulatory effector PRMT5-deficient T cells. Notably, IL-2 signaling is known to negatively impact Tfh differentiation. Collectively, our findings identify PRMT5 as a prominent regulator of Tfh programming, with potential causal links to IL-2 signaling.