The SEB1741 Aptamer Is an Efficient Tool for Blocking CD4+ T Cell Activation Induced by Staphylococcal Enterotoxin B

Author:

Chavez-Galan Leslie1ORCID,Ruiz Andy1ORCID,Ramón-Luing Lucero A.1ORCID,Escamilla-Gutiérrez Alejandro23,Sánchez-Monciváis Anahí4ORCID,Tecuatzi-Cadena Brenda4,Medina-Quero Karen4ORCID,Córdova-Espinoza María Guadalupe24ORCID

Affiliation:

1. Laboratory of Integrative Immunology, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico

2. Laboratory of Medical Bacteriology, Department of Microbiology, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City 11350, Mexico

3. Hospital General “Dr. Gaudencio González Garza”, Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social IMSS, Mexico City 02990, Mexico

4. Laboratory of Immunology, Escuela Militar de Graduados de Sanidad, SEDENA, Mexico City 11200, Mexico

Abstract

Staphylococcal enterotoxin B (SEB) is a protein produced by Staphylococcus aureus, which is toxic to humans. It is well known for its ability to stimulate the exacerbated activation of proinflammatory CD4+ T cells (Th1 profile), and in vitro studies have been conducted to understand its mechanism of action and its potential use as an immune therapy. However, the efficiency of the SEB1741 aptamer in blocking SEB has not been experimentally demonstrated. Methods: Enrichment CD4+ T cells were stimulated with SEB, and as a blocker, we used the SEB1741 aptamer, which was previously synthesised by an “in silico” analysis, showing high affinity and specificity to SEB. The efficiency of the SEB1741 aptamer in blocking CD4+ T cell activation was compared with that of an anti-SEB monoclonal antibody. Flow cytometry and Bio-Plex were used to evaluate the T-cell function. Results: In vitro, SEB induced the activation of CD4+ T cells and favoured a Th1 profile; however, the SEB1741 aptamer was highly efficient in decreasing the frequency of CD4+ T cells positive to ki-67 and CD69 cells, this means that proliferation and activation of CD4+ T cells was decreased. Moreover, the production of interleukin 2 (IL-2) and interferon-gamma (IFN-γ) was affected, suggesting that the Th1 profile is not present when the SEB1441 aptamer is used. Thus, the SEB1741 function was similar to that of anti-SEB. Conclusions: The SEB1741 aptamer is a valuable tool for blocking CD4+ T cell activation and the subsequent release of proinflammatory cytokines by SEB stimulation.

Publisher

MDPI AG

Subject

Chemistry (miscellaneous),Analytical Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Molecular Medicine,Drug Discovery,Pharmaceutical Science

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