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J. Exp. Med.,
Volume 187, Number 4, February 16, 1998 469-477
By
From the * Molecular Immunology, Swiss Tropical Institute, Basel, CH-4002, Switzerland; the During immune responses the initial activation of B cells takes place in T cell zones of periarteriolar lymphoid sheaths (PALS) of the splenic white pulp. After initial activation, B cells migrate into the primary follicles and, in association with follicular dendritic cells (FDCs), undergo clonal expansion and differentiation giving rise to germinal centers (GCs). Peanut
agglutinin binding (PNA+) cells of the GC differentiate further into memory or plasma cells.
Here we report that in tumor necrosis factor receptor 1-deficient mice (TNFR1 Institute of Pathology, University of Basel, Basel, CH-4003, Switzerland; the § Department of Viral
and Genetic Therapeutics, Chiron Technologies, San Diego, California 92121; the Geneva
Biomedical Research Institute, Plan-les-Ouates, CH-1228, Switzerland; and the ¶ Basel Institute for
Immunology, Basel, CH-4005, Switzerland
/), the location of B cells was altered and that plasma cells were abnormally distributed in the splenic
PALS. In contrast to lymphotoxin 
-deficient mice (LT/), bone marrow or fetal liver
transplantation did not correct the abnormal organization of the spleen, location of B cells, the
lack of an FDC network, nor the antibody response in TNFR1/ mice. These results argue
for a crucial role of TNFR1 expression on nonhematopoietic cells for the maintenance of the
splenic architecture and proper B cell location. In addition, the lack in development of an FDC
network after adoptive transfer suggests that either FDCs are not of bone marrow origin or that
they depend on signals from nonhematopoietic cells for maturation.
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