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MicroRNA expression profiles in human CD3(+) T cells following stimulation with anti-human CD3 antibodies

BACKGROUND: Anti-CD3 therapy can induce immunosuppression by several non mutually exclusive mechanisms that have been proposed to explain the therapeutic effect the administration anti-CD3 mAb, but its immunoregulatory mechanism is still not completely clear. In T cells, microRNAs (miRNAs) regulate...

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Detalles Bibliográficos
Autores principales: Sousa, Isabel Garcia, do Almo, Manuela Maragno, Simi, Kelly Cristina Rodrigues, Bezerra, Maryani Andressa Gomes, Andrade, Rosângela Vieira, Maranhão, Andréa Queiroz, Brigido, Marcelo Macedo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5351193/
https://www.ncbi.nlm.nih.gov/pubmed/28292330
http://dx.doi.org/10.1186/s13104-017-2442-y
Descripción
Sumario:BACKGROUND: Anti-CD3 therapy can induce immunosuppression by several non mutually exclusive mechanisms that have been proposed to explain the therapeutic effect the administration anti-CD3 mAb, but its immunoregulatory mechanism is still not completely clear. In T cells, microRNAs (miRNAs) regulate several pathways, including those associated with immune tolerance. Here, we report changes in miRNA expression in T cells following treatment with anti-human CD3 antibodies. Peripheral blood mononuclear cells were cultured in the presence of the monoclonal antibody OKT3 or a recombinant fragment of humanized anti-CD3. Following these treatments, the expression profiles of 31 miRNA species were assessed in T cells using TaqMan arrays. RESULTS: Eight of the tested miRNAs (miR-155, miR-21, miR-146a, miR-210, miR-17, miR-590-5p, miR-106b and miR-301a) were statistically significantly up- or down-regulated relative to untreated cells. CONCLUSIONS: Stimulation of T cells with anti-human CD3 antibodies alters miRNA expression patterns, including of miRNA species associated with immune regulatory pathways. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13104-017-2442-y) contains supplementary material, which is available to authorized users.