| First Author | Christensen JP | Year | 1996 |
| Journal | J Virol | Volume | 70 |
| Issue | 12 | Pages | 8997-9002 |
| PubMed ID | 8971031 | Mgi Jnum | J:36604 |
| Mgi Id | MGI:84032 | Doi | 10.1128/jvi.70.12.8997-9002.1996 |
| Citation | Christensen JP, et al. (1996) T-cell-mediated immunity to lymphocytic choriomeningitis virus in beta2-integrin (CD18)- and ICAM-1 (CD54)-deficient mice. J Virol 70(12):8997-9002 |
| abstractText | The T-cell response to lymphocytic choriomeningitis virus was studied in mice with deficient expression of beta2-integrins or ICAM-1. In such mice, the generation of virus-specific cytotoxic T lymphocytes was only slightly impaired and bystander activation was as extensive as that observed in wild-type mice. T-cell-mediated inflammation, assessed as primary footpad swelling and susceptibility to intracerebral infection, was slightly compromised only in beta2-integrin-deficient mice. However, adoptive immunization of mutant mice soon after local infection did reveal a reduced capacity to support the inflammatory reaction, indicating that under conditions of more limited immune activation both molecules do play a role in formation of the inflammatory exudate. Finally, virus control was found to be somewhat impaired in both mutant strains. In conclusion, our results indicate that although LFA-1-ICAM-1 interaction is important for certain aspects of the T-cell-mediated response to viruses, T-cell activation is surprisingly intact in these mutant mice, indicating extensive functional redundancy within cell interaction molecules. |
