These authors contributed equally to this work.
Inhibition of a C-rich oligodeoxynucleotide on activation of immune cells in vitro and enhancement of antibody response in mice
Article first published online: 15 JUL 2010
© 2010 The Authors. Immunology © 2010 Blackwell Publishing Ltd
Volume 131, Issue 4, pages 501–512, December 2010
How to Cite
Yang, G., Wan, M., Zhang, Y., Sun, L., Sun, R., Hu, D., Zhou, X., Wang, L., Wu, X., Wang, L. and Yu, Y. (2010), Inhibition of a C-rich oligodeoxynucleotide on activation of immune cells in vitro and enhancement of antibody response in mice. Immunology, 131: 501–512. doi: 10.1111/j.1365-2567.2010.03322.x
- Issue published online: 4 NOV 2010
- Article first published online: 15 JUL 2010
- Received 22 March 2010; revised 14 May 2010; accepted 20 May 2010.
- autoimmune disease;
- suppressive oligodeoxynucleotides;
- toll like receptor;
- type I interferon
To explore the possibility that human mitochondrial genomic DNA-mimicking oligodeoxynucleotides could regulate the immune response, a series of mitochondrial DNA-based oligodeoxynucleotides (MTODNs) were designed and studied to determine their immunoregulatory effects on immune cells activated by toll-like receptor (TLR) stimulation. The results showed that a C-rich MTODN, designated MT01, was able to inhibit the proliferation of human peripheral blood mononuclear cells (PBMCs) induced by cytosine–phosphate–guanosine (CpG) oligodeoxynucleotides (ODNs) and the production of type I interferon (IFN) from human PBMCs stimulated by TLR agonists, including inactivated influenza virus, imiquimod, inactivated herpes simplex virus-1 (HSV-1) and CpG ODNs. In addition, MT01 inhibited the CpG ODN-enhanced antibody response and this inhibition could be related to the antagonism of TLR9-activation pathways in B cells. Notably, unlike the G-rich suppressive ODNs reported, MT01 is composed of ACCCCCTCT repeats. These data imply that MT01 represents a novel class of immunosuppressive ODNs that could be candidate biologicals with therapeutic use in TLR activation-associated diseases.