B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity

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B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity. / Moseman, E.A.; Iannacone, M.; Bosurgi, L.; Tonti, E.; Chevrier, N.; Tumanov, A.; Fu, Y.-X.; Hacohen, N.; von Andrian, U.

in: IMMUNITY, Jahrgang 36, Nr. 3, 2012, S. 415-426.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Moseman, EA, Iannacone, M, Bosurgi, L, Tonti, E, Chevrier, N, Tumanov, A, Fu, Y-X, Hacohen, N & von Andrian, U 2012, 'B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity', IMMUNITY, Jg. 36, Nr. 3, S. 415-426. https://doi.org/10.1016/j.immuni.2012.01.013

APA

Moseman, E. A., Iannacone, M., Bosurgi, L., Tonti, E., Chevrier, N., Tumanov, A., Fu, Y-X., Hacohen, N., & von Andrian, U. (2012). B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity. IMMUNITY, 36(3), 415-426. https://doi.org/10.1016/j.immuni.2012.01.013

Vancouver

Bibtex

@article{5a1c4237b2ad4b999213294aeab0a9d7,
title = "B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity",
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.",
author = "E.A. Moseman and M. Iannacone and L. Bosurgi and E. Tonti and N. Chevrier and A. Tumanov and Y.-X. Fu and N. Hacohen and {von Andrian}, U.",
year = "2012",
doi = "10.1016/j.immuni.2012.01.013",
language = "English",
volume = "36",
pages = "415--426",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity

AU - Moseman, E.A.

AU - Iannacone, M.

AU - Bosurgi, L.

AU - Tonti, E.

AU - Chevrier, N.

AU - Tumanov, A.

AU - Fu, Y.-X.

AU - Hacohen, N.

AU - von Andrian, U.

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?eid=2-s2.0-84858761664&partnerID=MN8TOARS

U2 - 10.1016/j.immuni.2012.01.013

DO - 10.1016/j.immuni.2012.01.013

M3 - SCORING: Journal article

C2 - 22386268

VL - 36

SP - 415

EP - 426

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 3

ER -