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Forschungszentrum Karlsruhe, Institute of Toxicology and Genetics, Karlsruhe, Germany
High levels of the Rel/NF-
B family member RelB are restricted to
specific regions of thymus, lymph nodes, and Peyer’s patches. In
spleen, RelB is expressed in periarteriolar lymphatic sheaths, germinal
centers (GCs), and the marginal zone (MZ). In this study, we report
that RelB-deficient (relB-/-) mice,
in contrast to nfkb1-/-, but similar
to nfkb2-/- mice, are unable to form
GCs and follicular dendritic cell networks upon Ag challenge in the
spleen. RelB is also required for normal organization of the MZ and its
population by macrophages and B cells. Reciprocal bone marrow transfers
demonstrate that RelB expression in radiation-resistant stromal cells,
but not in bone marrow-derived hemopoietic cells, is required for
proper formation of GCs, follicular dendritic cell networks, and MZ
structures. However, the generation of MZ B cells requires RelB in
hemopoietic cells. Expression of TNF ligand/receptor family members is
only moderately altered in relB-/-
splenocytes. In contrast, expression of homing chemokines is strongly
reduced in relB-/- spleen with
particularly low mRNA levels of the chemokine B lymphocyte
chemoattractant. Our data indicate that activation of p52-RelB
heterodimers in stromal cells downstream of TNF/lymphotoxin is required
for normal expression of homing chemokines and proper development of
spleen microarchitecture.
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