Gene therapy for arthritis

May 15, 2001

The ability of immune cells to home to peripheral lymphoid organs or target tissues is critical to autoimmune patho-genesis, but it also makes these cells a promising vehicle for delivering therapeutic agents to the relevant tissues. Two reports in this issue apply this principle to suppress collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis. Nakajima and colleagues previously used adoptive transfer of transgenic T cells to block autoimmune responses in the CNS, and here they employ a similar strategy, transducing collagen-specific helper T cells with an antagonist of the cytokine IL-12. They introduce the modified T cells into mice that would otherwise develop CIA and show that the cells home efficiently to the synovium and block inflammation in situ. In contrast, their CNS-directed T cells, which express the same immunosuppressive transgene and are effective against a different autoim-mune disease, do not persist in the synovium and fail to suppress arthritis. In a complementary effort, Morita et al. show that dendritic cells (DCs), which control the proliferation and immunological properties of T cells, can also be used to deliver an appropriate regulatory protein. These authors generated DCs, transduced them with IL-4, and rein-troduced them into mice. The modified DCs can interact with collagen-specific T cells and drive them toward the Th2 phenotype, which is associated with tolerance to the corresponding antigens. Here again, tissue targeting is cru-cial, since the DCs must reach the spleen if they are to have their desired effect on T-cell development. Morita et al. show that delivery by intraperitoneal injection leads to the most efficient targeting of DCs to the spleen and confers the greatest protection from arthritis.

JCI Journals

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