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, Vol. 36, No. 3, 2012, p. 415-426.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -