| First Author | Martin DL | Year | 2010 |
| Journal | Infect Immun | Volume | 78 |
| Issue | 7 | Pages | 3154-9 |
| PubMed ID | 20457790 | Mgi Jnum | J:160974 |
| Mgi Id | MGI:4456897 | Doi | 10.1128/IAI.00275-10 |
| Citation | Martin DL, et al. (2010) Generation of Trypanosoma cruzi-specific CD8(+) T-cell immunity is unaffected by the absence of type I interferon signaling. Infect Immun 78(7):3154-9 |
| abstractText | Trypanosoma cruzi is a protozoan parasite that causes human Chagas' disease, a leading source of congestive heart failure in Central and South America. CD8(+) T cells are critical for control of T. cruzi infection, and CD8(+) T cells recognizing the immunodominant trans-sialidase gene-encoded peptide TSKB20 (ANYKFTLV) account for approximately 30% of the total CD8(+) T-cell population at the peak of infection in C57BL/6 mice. Type I interferons (IFN-I) are pleiotropic cytokines that play a critical role in both innate and adaptive immunity against a variety of infections, but their induction and their role in infection are dictated by the infectious agent. Because type I IFNs and IFN-responsive genes are evident early after T. cruzi infection of host cells, we examined the influence of IFN-I on the development of CD8(+) T-cell responses during this infection. Mice lacking the receptor for IFN-I (IFNARKO) and their wild-type counterparts both developed chronic infections and generated similar frequencies of immunodominant TSKB20- and subdominant TSKB18-specific CD8(+) T cells following T. cruzi infection. In contrast, peak TSKB20-specific CD8(+) T-cell responses generated during infection with vaccinia virus engineered to express TSKB20 were approximately 2.5-fold lower in IFNARKO mice than B6 mice, although after viral clearance, the frequencies of TSKB20-specific CD8(+) T cells stabilized at similar levels. Together, these data suggest that IFN-I induction and biology are dependent upon the microbial context and emphasize the need to investigate various infection models for a full understanding of CD8(+) T-cell development. |
