| Autor: |
Eaton-Fitch N; National Centre for Neuroimmunology and Emerging Diseases.; Consortium Health International for Myalgic Encephalomyelitis, and., Rudd P; Institute for Biomedicine and Glycomics, Griffith University, Gold Coast, Australia., Er T; School of Human Sciences (Physiology), The University of Western Australia, Perth, Australia., Hool L; School of Human Sciences (Physiology), The University of Western Australia, Perth, Australia.; Victor Chang Cardiac Institute, Australia., Herrero L; Institute for Biomedicine and Glycomics, Griffith University, Gold Coast, Australia., Marshall-Gradisnik S; National Centre for Neuroimmunology and Emerging Diseases.; Consortium Health International for Myalgic Encephalomyelitis, and. |
| Jazyk: |
angličtina |
| Zdroj: |
JCI insight [JCI Insight] 2024 Oct 22; Vol. 9 (20). Date of Electronic Publication: 2024 Oct 22. |
| DOI: |
10.1172/jci.insight.183810 |
| Abstrakt: |
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and long COVID are debilitating multisystemic conditions sharing similarities in immune dysregulation and cellular signaling pathways contributing to the pathophysiology. In this study, immune exhaustion gene expression was investigated in participants with ME/CFS or long COVID concurrently. RNA was extracted from peripheral blood mononuclear cells isolated from participants with ME/CFS (n = 14), participants with long COVID (n = 15), and healthy controls (n = 18). Participants with ME/CFS were included according to Canadian Consensus Criteria. Participants with long COVID were eligible according to the case definition for "Post COVID-19 Condition" published by the World Health Organization. RNA was analyzed using the NanoString nCounter Immune Exhaustion gene expression panel. Differential gene expression analysis in ME/CFS revealed downregulated IFN signaling and immunoglobulin genes, and this suggested a state of immune suppression. Pathway analysis implicated dysregulated macrophage activation, cytokine production, and immunodeficiency signaling. Long COVID samples exhibited dysregulated expression of genes regarding antigen presentation, cytokine signaling, and immune activation. Differentially expressed genes were associated with antigen presentation, B cell development, macrophage activation, and cytokine signaling. This investigation elucidates the intricate role of both adaptive and innate immune dysregulation underlying ME/CFS and long COVID, emphasizing the potential importance of immune exhaustion in disease progression. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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