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Blood, 1 October 2000, Vol. 96, No. 7, pp. 2338-2345
CHEMOKINES
Regulation of CCR6 chemokine receptor expression and
responsiveness to macrophage inflammatory protein-3 /CCL20 in human
B cells
Roman Krzysiek,
Eric A. Lefevre,
Jérôme Bernard,
Arnaud Foussat,
Pierre Galanaud,
Fawzia Louache, and
Yolande Richard
From the Institut National de la Santé et de la
Recherche Médicale (INSERM) U 131, Institut Paris-Sud sur les
Cytokines, Clamart, France; and INSERM U 362, Institut
Gustave Roussy, Villejuif, France.
The regulation of CCR6 (chemokine receptor 6) expression during
B-cell ontogeny and antigen-driven B-cell differentiation was analyzed.
None of the CD34+Lin hematopoietic stem cell
progenitors or the CD34+CD19+ (pro-B) or the
CD19+CD10+ (pre-B/immature B cells) B-cell
progenitors expressed CCR6. CCR6 is acquired when CD10 is lost and
B-cell progeny matures, entering into the surface immunoglobulin
D+ (sIgD+) mature B-cell pool. CCR6 is
expressed by all bone marrow-, umbilical cord blood-, and peripheral
blood-derived naive and/or memory B cells but is absent from germinal
center (GC) B cells of secondary lymphoid organs. CCR6 is
down-regulated after B-cell antigen receptor triggering and remains
absent during differentiation into immunoglobulin-secreting plasma
cells, whereas it is reacquired at the stage of post-GC memory B cells.
Thus, within the B-cell compartment, CCR6 expression is restricted to
functionally mature cells capable of responding to antigen challenge.
In transmigration chemotactic assays, macrophage inflammatory protein
(MIP)-3 /CC chemokine ligand 20 (CCL20) induced vigorous migration of
B cells with differential chemotactic preference toward
sIgD memory B cells. These data suggest that restricted
patterns of CCR6 expression and MIP-3 /CCL20 responsiveness
are integral parts of the process of B-lineage maturation and
antigen-driven B-cell differentiation.

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