T-cell-mediated immunity to lymphocytic choriomeningitis virus in beta2-integrin (CD18)- and ICAM-1 (CD54)-deficient mice
Research output: Contribution to journal › Journal article › Research › peer-review
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.
Original language | English |
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Journal | Journal of Virology |
Volume | 70 |
Issue number | 12 |
Pages (from-to) | 8997-9002 |
Number of pages | 5 |
ISSN | 0022-538X |
Publication status | Published - 1996 |
Bibliographical note
Keywords: Animals; Antigens, CD18; Gene Deletion; Hypersensitivity, Delayed; Immunity, Cellular; Inflammation; Intercellular Adhesion Molecule-1; Lymphocyte Activation; Lymphocytic choriomeningitis virus; Mice; T-Lymphocytes, Cytotoxic
ID: 9639767