Perturbation of effector and regulatory T cell subsets in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) (2019) Karhan, Unutmaz et al

OK Derya Unutmaz answered, he is checking it and will get back. He also said about posting soon a revised version of the paper. This table (Supplemental table 2 which i could not find in the paper) is very important i think, because it shows the features used for the machine learning algorithm used to classify between ME patients and controls.
 
Is low cd8, cd8 lymphopenia a frequent finding in me/cfs?

Hi butter, we have a few threads on this subject. It seems some pwME CD8 counts are high, while others are low. It varies. Mine are below normal range.
 
MAIT cell activation and dynamics associated with COVID-19 disease severity

https://immunology.sciencemag.org/content/5/51/eabe1670.full

Severe COVID-19 is characterized by excessive inflammation of the lower airways. The balance of protective versus pathological immune responses in COVID-19 is incompletely understood. Mucosa-associated invariant T (MAIT) cells are antimicrobial T cells that recognize bacterial metabolites, and can also function as innate-like sensors and mediators of antiviral responses. Here, we investigated the MAIT cell compartment in COVID-19 patients with moderate and severe disease, as well as in convalescence. We show profound and preferential decline in MAIT cells in the circulation of patients with active disease paired with strong activation. Furthermore, transcriptomic analyses indicated significant MAIT cell enrichment and pro-inflammatory IL-17A bias in the airways. Unsupervised analysis identified MAIT cell CD69high and CXCR3low immunotypes associated with poor clinical outcome. MAIT cell levels normalized in the convalescent phase, consistent with dynamic recruitment to the tissues and later release back into the circulation when disease is resolved. These findings indicate that MAIT cells are engaged in the immune response against SARS-CoV-2 and suggest their possible involvement in COVID-19 immunopathogenesis.
 
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