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  • Open Access

Modulation of the immune response in HTLV-1-infections by SM29 antigen in vitro is dependent of IL-10, TGF-β and CTLA-4

  • 1,
  • 1,
  • 1,
  • 1,
  • 2,
  • 2,
  • 3,
  • 1 and
  • 1Email author
Retrovirology201411 (Suppl 1) :P68

https://doi.org/10.1186/1742-4690-11-S1-P68

  • Published:

Keywords

  • Immune Response
  • Cell Culture
  • Infectious Disease
  • Inflammatory Response
  • Cancer Research

The HTLV-1 is the causal agent of HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). The immune response in HTLV-1 infection is polarized to the Th1-type, and previous data from our group had demonstrated that the use of Schistosoma antigens to cell cultures in HTLV-1 infection resulted in down-modulation of Th1/inflammatory response. The aim of this study was to evaluate whether the modulation of inflammatory response by S. mansoni antigens depends upon the presence of IL-10, TGF-β and CTLA-4. The antibodies anti-IL-10, anti-TGF-β and anti-CTLA-4 with or without the S. mansoni antigen Sm29 were added to the PBMC cultures of HTLV-1- infected individuals and the levels of cytokines in the supernatants were measure using ELISA sandwich method. Compared to the levels of cytokine in non stimulated cultures (1.073 pg/ml, median values), the levels of IFN-gproduction (552 pg/ml, 1.002 pg/ml and 548 pg/ml, respectively; p<0.05). On the other hand, the levels of IL-10 were increased by the presence of Sm29 (it passed from 26 pg/ml to102 pg/ml; p=0.02), however when anti-TGF-β and anti-CTLA-4 were added to the cultures there was a reduction in the levels of IL-10 (19 pg/ml and 23 pg/ml, respectively; p<0.05). The regulation of IFN-y production by Sm29 antigen in HTLV-1-infected individuals is dependent on IL-10, TGF-β and CTLA-4. Also the levels of IL-10 were affected by the neutralization of TGF-β and CTLA-4.

Financial support

CNPQ (Universal 479417/2008 3), NIH (R01AI079238A).

Authors’ Affiliations

(1)
Serviço de Imunologia, Hospital Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador-BA, Brazil
(2)
Instituto de Ciências Biológicas, Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte-MG, Brazil
(3)
Division of Infectious Diseases, Queensland Institute of Medical Research, Brisbane, Queensland, Australia

Copyright

© Lima et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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