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Department of Immunology, Duke University Medical Center, Durham, NC 27710
B lymphocytes are critically regulated by signals transduced
through the CD19-CD21 cell surface receptor complex, where complement
C3d binding to CD21 supplies an already characterized ligand. To
determine the extent that CD19 function is controlled by complement
activation, CD19-deficient mice (that are hyporesponsive to
transmembrane signals) and mice overexpressing CD19 (that are
hyperresponsive) were crossed with CD21- and C3-deficient mice. Cell
surface CD19 and CD21 expression were significantly affected by the
loss of CD21 and C3 expression, respectively. Mature B cells from
CD21-deficient littermates had 
36% higher cell surface CD19
expression, whereas CD21/35 expression was increased by 45% on B
cells from C3-deficient mice. Negative regulation of CD19 and CD21
expression by CD21 and C3, respectively, may be functionally
significant because small increases in cell surface CD19 overexpression
can predispose to autoimmunity. Otherwise, B cell development and
function in CD19-deficient and -overexpressing mice were not
significantly affected by a simultaneous loss of CD21 expression.
Although CD21-deficient mice were found to express a hypomorphic cell
surface CD21 protein at low levels that associated with mouse CD19, C3
deficiency did not significantly affect B cell development and function
in CD19-deficient or -overexpressing mice. These results, and the
severe phenotype exhibited by CD19-deficient mice compared with CD21-
or C3-deficient mice, collectively demonstrate that CD19 can regulate B
cell signaling thresholds independent of CD21 engagement and complement
activation.
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