Lack of specific T- and B-cell clonal expansions in multiple sclerosis patients with progressive multifocal leukoencephalopathy.
Diego BertoliAlessandra SottiniRuggero CapraCristina ScarpazzaRoberto BrescianiLuigi Daniele NotarangeloLuisa ImbertiPublished in: Scientific reports (2019)
Progressive multifocal leukoencephalopathy (PML) is a rare, potentially devastating myelin-degrading disease caused by the JC virus. PML occurs preferentially in patients with compromised immune system, but has been also observed in multiple sclerosis (MS) patients treated with disease-modifying drugs. We characterized T and B cells in 5 MS patients that developed PML, 4 during natalizumab therapy and one after alemtuzumab treatment, and in treated patients who did not develop the disease. Results revealed that: i) thymic and bone marrow output was impaired in 4 out 5 patients at the time of PML development; ii) T-cell repertoire was restricted; iii) clonally expanded T cells were present in all patients. However, common usage or pairings of T-cell receptor beta variable or joining genes, specific clonotypes or obvious "public" T-cell response were not detected at the moment of PML onset. Similarly, common restrictions were not found in the immunoglobulin heavy chain repertoire. The data indicate that no JCV-related specific T- and B-cell expansions were mounted at the time of PML. The current results enhance our understanding of JC virus infection and PML, and should be taken into account when choosing targeted therapies.
Keyphrases
- multiple sclerosis
- end stage renal disease
- bone marrow
- white matter
- newly diagnosed
- chronic kidney disease
- ejection fraction
- prognostic factors
- peritoneal dialysis
- mesenchymal stem cells
- machine learning
- oxidative stress
- patient reported outcomes
- electronic health record
- dna damage
- dna methylation
- genome wide
- replacement therapy
- high throughput sequencing
- deep learning