miR-15a and 16-1 Are Downregulated in CD4+ T Cells of Multiple Sclerosis Relapsing Patients

ABSTRACT The pathology of relapsing-remitting multiple sclerosis (RR-MS) is largely attributed to activated autoreactive effector T lymphocytes. The influence of microRNAs on the immune response has been shown to occur in different pathways of lymphocyte differentiation and function. Here, the expre...

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Published in:International journal of neuroscience 2012-08, Vol.122 (8), p.466-471
Main Authors: Lorenzi, Julio Cesar Cetrulo, Brum, Doralina G., Zanette, Dalila L., de Paula Alves Souza, Alessandra, Barbuzano, Fernanda Gonçalves, dos Santos, Antonio Carlos, Barreira, Amilton Antunes, da Silva, Wilson Araujo
Format: Article
Language:English
Subjects:
Adult
apoptosis
BCL-2
Case-Control Studies
CD4-Positive T-Lymphocytes - metabolism
CD8-Positive T-Lymphocytes - metabolism
Cell Proliferation
Disability Evaluation
Down-Regulation - immunology
Female
Humans
Lymphocyte Activation - immunology
lymphocytes
Male
MicroRNAs - genetics
MicroRNAs - metabolism
miRNAs
Multiple Sclerosis, Relapsing-Remitting - genetics
Multiple Sclerosis, Relapsing-Remitting - immunology
Multiple Sclerosis, Relapsing-Remitting - metabolism
Proto-Oncogene Proteins c-bcl-2 - metabolism
RNA, Messenger - metabolism
Young Adult
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Summary:ABSTRACT The pathology of relapsing-remitting multiple sclerosis (RR-MS) is largely attributed to activated autoreactive effector T lymphocytes. The influence of microRNAs on the immune response has been shown to occur in different pathways of lymphocyte differentiation and function. Here, the expression of the miRNAs miR-15a/16-1 in PBMC, CD4+, and CD8+ from RR-MS patients has been investigated. BCL2, a known miR-15a/16-1 target, has also been analyzed. The results have shown that miR-15a/16-1 is downregulated in CD4+ T cells, whereas BCL2 is highly expressed in RR-MS patients only. Our data suggest that miR-15a/16-1 can also modulate the BCL2 gene expression in CD4+ T cells from RR-MS patients, thereby affecting apoptosis processes.
ISSN:0020-7454
1563-5279
1543-5245
DOI:10.3109/00207454.2012.678444