Expression of Akt1 and p-Akt1 in peripheral T cell subsets of multiple sclerosis patients
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ORIGINAL ARTICLE
Expression of Akt1 and p‑Akt1 in peripheral T cell subsets of multiple sclerosis patients Fatma Betul Oktelik1 · Vuslat Yilmaz2 · Recai Turkoglu3 · Ece Akbayir2 · Erdem Tuzun2 · Gunnur Deniz1 · Suzan Cinar1 Received: 11 June 2020 / Accepted: 28 September 2020 © Belgian Neurological Society 2020
Abstract Multiple sclerosis is an autoimmune disorder induced by the infiltration of autoreactive immune cells into the central nervous system. Akt/PKB signaling pathway is crucially involved in T cell development and survival. We aimed to determine whether Akt1 expression levels of regulatory T (Treg) cells are altered in MS and are associated with disease activity. Relapsing–remitting multiple sclerosis (RR-MS, n = 17) patients and healthy individuals (n = 20) were enrolled. Peripheral blood mononuclear cells were isolated and anti-CD3, -CD4, -CD8, -CD25, -CD127 monoclonal antibodies were used to identify the T cell subsets. After stimulation with phorbol myristate acetate/ionomycin, the Akt1 and phosphorylated-Akt1 (p-Akt1) levels of T cell subsets were detected with intracellular staining using flow cytometry. Total Akt1 and p-Akt1 expression levels were found to be suppressed in C D4+ T cell and Treg populations of RR-MS patients. Progression indices were positively correlated with Akt1 expression levels of Tregs indicating that the Akt pathway might partake in the progression of multiple sclerosis. Flow cytometry may effectively be used for the evaluation of the Akt pathway activity. Our findings suggest that the magnitude of suppression of the Akt pathway might serve as a biomarker for the prognosis of multiple sclerosis. Keywords Multiple sclerosis · Phospho-Akt1 · Akt1 · Protein kinase B · Regulatory T cells Abbreviations MS Multiple sclerosis p-Akt1 Phosphorylated Akt1 PBMC Peripheral Blood Mononuclear Cell RR-MS Relapsing–Remitting MS Th T Helper Cells Treg Regulatory T Cells
Suzan Cinar and Fatma Betul Oktelik contributed equally to this work.
Introduction Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system, primarily mediated by T lymphocytes, particularly C D4+ helper T cells (Th) [1]. T cell activation occurs via signaling pathways such as JAK/STAT, Akt/mTor, Map Kinase and Nuclear factor κβ (NF-κβ). The families of Janus kinase (JAK) and signal transductors and activators of transcription (STAT) promote cytokine-mediated cell activation. The association between
* Suzan Cinar [email protected]; [email protected]
Gunnur Deniz [email protected]
Fatma Betul Oktelik [email protected]
1
Vuslat Yilmaz [email protected]
Department of Immunology, Istanbul University, Aziz Sancar Institute of Experimental Medicine, Vakif Gureba C. Fatih, Istanbul, Turkey
2
Recai Turkoglu [email protected]
Department of Neuro Science, Istanbul University, Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkey
3
Department of Neurology, Istanbul Haydarpasa Numune Training and Research Hospital, Istanbul,
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