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Comment
. 2012 Mar 23;36(3):315-7.
doi: 10.1016/j.immuni.2012.02.011.

B cells, not just for antibody anymore

Kamal M Khanna  1 , Leo Lefrançois
Affiliations
Comment

B cells, not just for antibody anymore

Kamal M Khanna et al. Immunity. .

Abstract

B cell antibody production is thought to be crucial for protection against virus infection. In this issue of Immunity, Moseman et al. (2012) illustrate an antibody-independent role for B cells in macrophage activation that prevents virus dissemination after subcutaneous infection.

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Figures

Figure 1
Figure 1
Following subcutaneous infection with VSV, the virus is initially captured by CD169+ macrophages in the draining lymph node. The release of LTα1β2 by B cells allows the CD169+ macrophages to tolerate increased replication of VSV, possibly by inducing Usp18. This increased VSV replication induces the release of IFNαβ by the CD169+ macrophages, which in turn prevents the virus from accessing the peripheral nerves and travelling to the CNS by an undefined mechanism. In the absence of B cells there is a lack of LTα1β2 and without this, the virus fails to replicate in the CD169+ macrophages, and IFNαβ secretion id severely diminished. The lack of IFNαβ allows the virus to access the peripheral nerves leading to dissemination of VSV to the CNS.
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References

    1. Benedict CA, Banks TA, Senderowicz L, Ko M, Britt WJ, Angulo A, Ghazal P, Ware CF. Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus detente. Immunity. 2001;15:617–626. - PubMed
    1. Ciavarra RP, Taylor L, Greene AR, Yousefieh N, Horeth D, van Rooijen N, Steel C, Gregory B, Birkenbach M, Sekellick M. Impact of macrophage and dendritic cell subset elimination on antiviral immunity, viral clearance and production of type 1 interferon. Virol. 2005;342:177–189. - PubMed
    1. Delale T, Paquin A, sselin-Paturel C, Dalod M, Brizard G, Bates EE, Kastner P, Chan S, Akira S, Vicari A, Biron CA, Trinchieri G, Briere F. MyD88-dependent and -independent murine cytomegalovirus sensing for IFN-alpha release and initiation of immune responses in vivo. J Immunol. 2005;175:6723–6732. - PubMed
    1. Edelson BT, Bradstreet TR, Hildner K, Carrero JA, Frederick KE, KCW, Belizaire R, Aoshi T, Schreiber RD, Miller MJ, Murphy TL, Unanue ER, Murphy KM. CD8alpha(+) dendritic cells are an obligate cellular entry point for productive infection by Listeria monocytogenes. Immunity. 2011;35:236–248. - PMC - PubMed
    1. Garcia-Sastre A, Biron CA. Type 1 interferons and the virus-host relationship: a lesson in detente. Science. 2006;312:879–882. - PubMed