Abstract:
: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.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Karrer U,Althage A,Odermatt B,Hengartner H,Zinkernagel RMdoi
10.1002/1521-4141(200010)30:10<2799::AID-IMMU2799>keywords:
subject
Has Abstractpub_date
2000-10-01 00:00:00pages
2799-807issue
10eissn
0014-2980issn
1521-4141pii
10.1002/1521-4141(200010)30:10<2799::AID-IMMU2799>journal_volume
30pub_type
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