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Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
07:07

Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice

Published on: June 27, 2020

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

Lisa M Sedger1, Sam Hou, Sarah R Osvath

  • 1Department of Molecular Immunology, Immunex, Seattle, WA 98101, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|November 22, 2002
PubMed

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 CD43(low/-)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-alpha, lymphotoxin-alpha, and both TNF receptors, TNFR1-p55 and TNFR2-p75. Thus, TNF-alpha and lymphotoxin-alpha are required for loss of BM B lineage cells during respiratory infection with influenza virus.

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