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Immunity. 2012 Mar 23;36(3):415-26. doi: 10.1016/j.immuni.2012.01.013. Epub 2012 Mar 1.

B cell maintenance of subcapsular sinus macrophages protects against a fatal viral infection independent of adaptive immunity.

Author information

1
Immune Disease Institute and Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.

Abstract

Neutralizing antibodies have been thought to be required for protection against acutely cytopathic viruses, such as the neurotropic vesicular stomatitis virus (VSV). Utilizing mice that possess B cells but lack antibodies, we show here that survival upon subcutaneous (s.c.) VSV challenge was independent of neutralizing antibody production or cell-mediated adaptive immunity. However, B cells were absolutely required to provide lymphotoxin (LT) α1β2, which maintained a protective subcapsular sinus (SCS) macrophage phenotype within virus draining lymph nodes (LNs). Macrophages within the SCS of B cell-deficient LNs, or of mice that lack LTα1β2 selectively in B cells, displayed an aberrant phenotype, failed to replicate VSV, and therefore did not produce type I interferons, which were required to prevent fatal VSV invasion of intranodal nerves. Thus, although B cells are essential for survival during VSV infection, their contribution involves the provision of innate differentiation and maintenance signals to macrophages, rather than adaptive immune mechanisms.

Comment in

PMID:
22386268
PMCID:
PMC3359130
DOI:
10.1016/j.immuni.2012.01.013
[Indexed for MEDLINE]
Free PMC Article

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