The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/2/469/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 4, February 16, 1998 469-477

Articles

Crucial Role of Tumor Necrosis Factor Receptor 1 Expression on Nonhematopoietic Cells for B Cell Localization within the Splenic White Pulp

Maria Tkachuk*, Stephan Bolliger{ddagger}, Bernhard Ryffel{ddagger}, Gerd Pluschke*, Theresa A. Banks§, Suzanne Herren||, Roland H. Gisler, and Marie H. Kosco-Vilbois||

From the * Molecular Immunology, Swiss Tropical Institute, Basel, CH-4002, Switzerland; the {ddagger} 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

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–/–), the location of B cells was altered and that plasma cells were abnormally distributed in the splenic PALS. In contrast to lymphotoxin {alpha}–deficient mice (LT{alpha}–/–), 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.

We are grateful to L. Dudler, B. Kugelberg, N. Favre, Drs. W. Hein, and G. Bordmann for excellent technical support. We thank Drs. A. Rolink and S. Takeda for generously providing antibodies, and C. Hebert for the production of the photomicrographs.

Basel Institute for Immunology was founded and is supported by F. Hoffmann-La Roche Ltd. (Basel, Switzerland).

Address correspondence to Marie H. Kosco-Vilbois, Geneva Biomedical Research Institute, 14 chemin des Aulx, Plan-les-Ouates, CH-1228, Switzerland. Phone: 041-022-706-9719, 706-9708; Fax: 041-022-794-6965; E-mail: marie.kosco-vilbois{at}serono.com; and Roland H. Gisler, Basel Institute for Immunology, Grenzacherstrasse 487, Basel, CH-4005, Switzerland. Phone: 041-061-605-1242; Fax: 041-061-605-1364; E-mail: gisler{at}bii.ch

1 Abbreviations used in this paper: BM, bone marrow; FDC, follicular dendritic cell; FL, fetal liver; GC, germinal center; LT-{alpha}, lymphotoxin {alpha}–deficient; PALS, periarteriolar lymphoid sheaths; PNA, peanut agglutinin; RT, room temperature; s, surface; SRBC, sheep red blood cell; WT, wild type.


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