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Journal of Immunology Research
Volume 2017, Article ID 2860867, 16 pages
https://doi.org/10.1155/2017/2860867
Research Article

B-CD8+ T Cell Interactions in the Anti-Idiotypic Response against a Self-Antibody

1Tumor Immunology Direction, Center of Molecular Immunology, Havana, Cuba
2Systems Biology Direction, Center of Molecular Immunology, Havana, Cuba
3Immunobiology Laboratory, Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research, New York, NY, USA

Correspondence should be addressed to Ana María Hernández; uc.dls.mic@atina

Received 4 August 2016; Revised 18 November 2016; Accepted 20 December 2016; Published 9 April 2017

Academic Editor: Gabriella Sarmay

Copyright © 2017 Darel Martínez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

P3 is a murine, germline, IgM mAb that recognizes N-glycolylated gangliosides and other self-antigens. This antibody is able to induce an anti-idiotypic IgG response and B-T idiotypic cascade, even in the absence of any adjuvant or carrier protein. P3 mAb immunization induces the expression of activation markers in a significant percentage of B-1a cells in vivo. Interestingly, transfer of both B-1a and B-2 to BALB/Xid mice was required to recover anti-P3 IgG response in this model. In fact, P3 mAb activated B-2 cells, in vitro, inducing secretion of IFN-γ and IL-4, although this activation was not detected ex vivo. Interestingly, naïve CD8+ T cells increased the expression of activation markers and IFN-γ secretion in the presence of B-1a cells isolated from P3 mAb-immunized mice, even without in vitro restimulation. In contrast, B-2 cells were able to stimulate CD8+ T cells only if P3 was added in vitro. Using bioinformatics, a MHC class I-binding peptide from P3 VH region was identified. P3 mAb was able to induce a specific CTL response in vivo against cells presenting this peptide. Both humoral and CTL anti-idiotypic responses could be mechanisms to protect against the self-reactive antibody, contributing to keeping the tolerance to self-antigens.