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| Content Provider | PubMed Central |
|---|---|
| Author | Kunzmann, Volker Kretzschmar, Eva Herrmann, Thomas Wilhelm, Martin |
| Copyright Year | 2004 |
| Abstract | The recognition of pathogen-associated molecular patterns (PAMPs) by the innate immune system is a crucial step in inducing effective immune responses. Double-stranded RNA [mimicked by polyinosinic-polycytidylic acid (poly(I:C)], synthesized by various types of viruses, represents one important member of these immunostimulatory microbial components. Here we report that poly(I:C) has potent γδ T-cell costimulatory capacity. Within peripheral blood mononuclear cells, poly(I:C)-stimulated γδ T cells expressed increased levels of CD69 and exhibited significantly enhanced antigen-mediated proliferation in response to isopentenylpyrophosphate (IPP). Among several recombinant cytokines tested, type I interferons (IFN-α, IFN-β) and interleukin-15 (IL-15) showed a similar activation pattern of γδ T cells. γδ T-cell clones and purified γδ T cells did not respond to poly(I:C), indicating indirect effects of this compound. Depletion of CD11c+ dendritic cells (DC), which express Toll-like receptor 3 (TLR3), known to recognize poly(I:C), abrogated poly(I:C)-mediated stimulation of γδ T cells. In addition, the supernatant of poly(I:C)-treated CD11c+ DC was able to mimic the stimulatory effects of poly(I:C) on γδ T cells. Experiments with neutralizing antibodies indicated that type I IFNs, but not IL-15, contributed to the poly(I:C)-mediated activation of γδ T cells. In conclusion, γδ T-cell activation by immunostimulatory double-stranded RNA, such as poly(I:C), is indirectly mediated via type I IFNs derived from TLR3-expressing CD11c+ DCs. These results suggest that upon confrontation with certain viruses, γδ T cells can be rapidly activated by type I interferons and may contribute to effective antiviral responses. |
| Related Links | http://dx.doi.org/10.1111/j.1365-2567.2004.01908.x |
| Ending Page | 377 |
| Page Count | 9 |
| Starting Page | 369 |
| File Format | |
| ISSN | 00192805 |
| e-ISSN | 13652567 |
| Journal | Immunology |
| Issue Number | 3 |
| Volume Number | 112 |
| Language | English |
| Publisher | Blackwell Science Inc |
| Publisher Date | 2004-07-01 |
| Access Restriction | Open |
| Rights Holder | Blackwell Science Inc |
| Subject Keyword | Immunology Immunology and Allergy Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Allergy Immunology |
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