Bone marrow B cell apoptosis during in vivo influenza virus infection requires TNF-α and lymphotoxin-α

Lisa M. Sedger, Sam Hou, Sarah R. Osvath, Moira B. Glaccum, Jacques J. Peschon, Nico Van Rooijen, Lisa Hyland*

*Corresponding author for this work

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Suppression of bone marrow myeloid and erythroid progenitor cells occurs after infection with a variety of different viruses. In this study, we characterize the alterations in bone marrow (BM) lymphocytes after influenza virus infection in mice. We found a severe loss of BM B cells, particularly CD43Blow/-B220+ pre-B and immature B cells, in influenza virus-infected mice. Depletion of BM B lineage cells resulted primarily from cell cycle arrest and most likely apoptosis within the BM environment, rather than from increased trafficking of BM emigrants to peripheral lymphoid tissues. Use of gene-knockout mice indicates that depletion of BM B cells is dependent on TNF-α lymphotoxin-α, and both TNF receptors, TNFR1-p55 and TNFR2-p75. Thus, TNF-α and lymphotoxin-α are required for loss of BM B lineage cells during respiratory infection with influenza virus.

Original languageEnglish
Pages (from-to)6193-6201
Number of pages9
JournalJournal of Immunology
Volume169
Issue number11
Publication statusPublished - 1 Dec 2002

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