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,§
*
Laboratory of Molecular Immunology, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, and Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow, Russia;
Intramural Research Support Program, Science Applications International Corp.-Frederick and Laboratory of Molecular Immunoregulation, Division of Basic Sciences, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD, 21702;
Institute of Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, Munich, Germany;
§
Institute for Genetics, University of Cologne, Cologne, Germany; and
¶
Department of Clinical Pathology, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702
Inactivation of genes encoding members of TNF and TNF receptor
families reveal their divergent roles in the formation and function of
secondary lymphoid organs. Most lymphotoxin 
(lt)-
and all lymphotoxin ß receptor (ltßr)-deficient mice
are completely devoid of lymph nodes (LNs); however, most lymphotoxin
ß (ltß)-deficient mice develop mesenteric LNs.
Tnf- and tnfrp55-deficient mice develop a
complete set of LNs, while ltß/tnfrp55
double-deficient mice lack all LNs, demonstrating cooperation between
LTß and TNFRp55 in LN development. Now we report that
ltß/tnf double-deficient mice develop the same set of
mucosal LNs as do ltß-deficient mice, suggesting that
ligands other than TNF signal through TNFRp55 during LN development.
These LNs retain distinct T and B cells areas; however, they lack
follicular dendritic cell networks. Structures resembling germinal
centers can be found in the LNs from immunized
ltß-deficient mice but not in ltß/tnf
double-deficient mice. Additionally, stromal components of the spleen
and LNs appear to be more severely disturbed in
ltß/tnf double-deficient mice as compared with
ltß-deficient mice. We conclude that LTß and TNF
cooperate in the establishment of the correct microarchitecture of
lymphoid organs.
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