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-Deficient Mice Alters the CXCL13/CCL19/CCL21 Ratio in the Spleen and Induces Maturation and Migration of Anergic B Cells into the B Cell Follicle1
*
Center for Immunology and
Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110; and
The Wistar Institute, Philadelphia, PA 19104
The organization of secondary lymphoid tissues into distinct T and
B cell compartments supports proper regulation of an immune response to
foreign Ags. In the splenic white pulp, this compartmentalization is
also thought to be important in the maintenance of B cell tolerance.
Using lymphotoxin-
-(LT-)-, TNF--, or TNFRp55-deficient mice,
all with disrupted splenic architecture, we tested whether normal T/B
segregation and/or intact follicular structure are necessary for the
maintenance of anti-dsDNA B cell anergy. This study demonstrates
that anti-dsDNA B cells remain tolerant in LT--/-,
TNF--/-, and TNFRp55-/- mice; however,
TNF- or a TNF--dependent factor is required for their
characteristic positioning to the T/B interface. Providing a TNF-
signal in TNF--/- mice by systemic administration of
an agonist anti-TNFRp55 mAb induces the maturation of the
anti-dsDNA B cells and their movement away from the T cell area
toward the B cell area. Additionally, the agonist Ab induces changes in
the follicular environment, including FDC clustering, up-regulation of
the CXC chemokine ligand CXCL13, and down-regulation of the CC
chemokine ligands CCL19 and CCL21. Therefore, this study suggests that
a balance between B and T cell tropic chemokine signals may be an
important mechanism for positioning anergic B cells at the T/B
interface of the splenic white pulp.
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