CD45 expression is essential for immunoglobulin (Ig)-mediated B cell activation. Treatments with either anti-Ig or anti-CD45 suggest that CD45 may facilitate early signaling events such as calcium mobilization, and phosphoinositide hydrolyis as well as later events leading to transcription of genes such as c-myc. To examine the role of CD45 more extensively, CD45-deficient mice were generated by disruption of exon 6. Although normal numbers of B cells were found in peripheral lymphoid tissues, CD45-deficient cells failed to proliferate upon IgM crosslinking. In the present study, we demonstrate that the fraction of high buoyant density B cells is reduced while low buoyant density cells are increased. Moreover, there is a significant decline in the number of splenic B cells of the mature IgDhi, IgMlo phenotype. Although both the basal and anti-Ig-induced levels of phosphorylation of Ig-alpha and phospholipase C gamma 2 are indistinguishable from that observed in CD45+ control B cells, a major distinction was found in Ca2+ mobilization. While anti-Ig-induced mobilization of intracellular Ca2+ stores was normal, influx from extracellular sources was abrogated. This finding reveals a novel pathway of regulating B cell responses mediated by CD45.
Article|
January 01 1996
Immunoglobulin-mediated signal transduction in B cells from CD45-deficient mice.
T Benatar,
T Benatar
Wellesley Hospital Research Institute, University of Toronto, Canada.
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R Carsetti,
R Carsetti
Wellesley Hospital Research Institute, University of Toronto, Canada.
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C Furlonger,
C Furlonger
Wellesley Hospital Research Institute, University of Toronto, Canada.
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N Kamalia,
N Kamalia
Wellesley Hospital Research Institute, University of Toronto, Canada.
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T Mak,
T Mak
Wellesley Hospital Research Institute, University of Toronto, Canada.
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C J Paige
C J Paige
Wellesley Hospital Research Institute, University of Toronto, Canada.
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T Benatar
Wellesley Hospital Research Institute, University of Toronto, Canada.
R Carsetti
Wellesley Hospital Research Institute, University of Toronto, Canada.
C Furlonger
Wellesley Hospital Research Institute, University of Toronto, Canada.
N Kamalia
Wellesley Hospital Research Institute, University of Toronto, Canada.
T Mak
Wellesley Hospital Research Institute, University of Toronto, Canada.
C J Paige
Wellesley Hospital Research Institute, University of Toronto, Canada.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1996) 183 (1): 329–334.
Citation
T Benatar, R Carsetti, C Furlonger, N Kamalia, T Mak, C J Paige; Immunoglobulin-mediated signal transduction in B cells from CD45-deficient mice.. J Exp Med 1 January 1996; 183 (1): 329–334. doi: https://doi.org/10.1084/jem.183.1.329
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