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Departments of Medicine and Immunology, Mayo Clinic, Rochester, MN 55905
Rheumatoid arthritis results from a T cell-driven inflammation in
the synovial membrane that is frequently associated with the formation
of tertiary lymphoid structures. The significance of this extranodal
lymphoid neogenesis is unknown. Microdissection was used to isolate CD4
T cells residing in synovial tissue T cell/B cell follicles. CD4 T
cells with identical TCR sequences were represented in independent,
nonadjacent follicles, suggesting recognition of the same Ag in
different germinal centers. When adoptively transferred into rheumatoid
arthritis synovium-SCID mouse chimeras, these CD4 T cell clones
enhanced the production of IFN-
, IL-1
, and TNF-
. In vivo
activity of adoptively transferred CD4 T cells required matching of
HLA-DRB1 alleles and also the presence of T cell/B
cell follicles. HLA-DRB1-matched synovial tissues that were
infiltrated by T cells, macrophages, and dendritic cells, but that
lacked B cells, did not support the activation of adoptively
transferred CD4 T cell clones, raising the possibility that B cells
provided a critical function in T cell activation or harbored the
relevant Ag. Dependence of T cell activation on B cells was confirmed
in B cell depletion studies. Treatment of chimeric mice with
anti-CD20 mAb inhibited the production of IFN- and IL-1,
indicating that APCs other than B cells could not substitute in
maintaining T cell activation. The central role of B cells in synovial
inflammation identifies them as excellent targets for immunosuppressive
therapy.
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