| First Author | Karrer U | Year | 2000 |
| Journal | Eur J Immunol | Volume | 30 |
| Issue | 10 | Pages | 2799-807 |
| PubMed ID | 11069060 | Mgi Jnum | J:65237 |
| Mgi Id | MGI:1913233 | Doi | 10.1002/1521-4141(200010)30:10<2799::AID-IMMU2799>3.0.CO;2-2 |
| Citation | Karrer U, et al. (2000) Immunodeficiency of alymphoplasia mice (aly/aly) in vivo: structural defect of secondary lymphoid organs and functional B cell defect. Eur J Immunol 30(10):2799-807 |
| abstractText | Alymphoplasia mice (aly/aly) have been shown to be deficient for a nuclear factor-kappaB-inducing kinase involved in signal transduction of lymphotoxin beta receptor (LT-betaR) and of CD40, resulting in structural defects of secondary lymphoid organs and highly increased susceptibility to viral infections. We analyzed the anti-viral immune response of bone marrow chimeras (BMC) between aly/aly mice and (C57BL/6 x DBA2)F1 mice (B6D2F1) to evaluate in vivo whether the structural defects of secondary lymphoid organs or intrinsic B or T cell defects led to immunodeficiency in aly/aly mice. Transfer of aly/aly bone marrow into B6D2F1 mice (aly/aly-->B6D2F1) led to excellent T but poor B cell reconstitution of recipients. Antiviral cytotoxic T cell (CTL) responses of aly/aly-->B6D2F1 BMC were clearly improved compared to aly/aly mice whereas virus-neutralizing IgG reponses were virtually absent. Therefore, the inefficient CTL response was predominantly caused by the structural defect of secondary lymphoid organs and not by an intrinsic T cell defect. In contrast, B cells of aly/aly origin were unable to undergo isotype switch after viral infections, indicating an intrinsic B cell defect in vivo. Overall, aly/aly mice show the combined immunodeficient phenotype of mice deficient for LT-3R with B cells functionally deficient for CD40. |
