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Control of the Autoimmune Response by Type 2 Nitric Oxide Synthase^{1 ,2}

Fu-Dong Shi^*, Malin Flodström^*, Soon Ha Kim^*, Shyam Pakala^*, Mary Cleary^*, Hans-Gustaf Ljunggren and Nora Sarvetnick^3,*

^* Department of Immunology, IMM-23, The Scripps Research Institute, La Jolla, CA 92037; and Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden

Immune defense against pathogens often requires NO, synthesized by type 2 NO synthase (NOS2). To discern whether this axis could participate in an autoimmune response, we immunized NOS2-deficient mice with the autoantigen acetylcholine receptor, inducing muscle weakness characteristic of myasthenia gravis, a T cell-dependent Ab-mediated autoimmune disease. We found that the acetylcholine receptor-immunized NOS2-deficient mice developed an exacerbated form of myasthenia gravis, and demonstrated that NOS2 expression limits autoreactive T cell determinant spreading and diversification of the autoantibody repertoire, a process driven by macrophages. Thus, NOS2/NO is important for silencing autoreactive T cells and may restrict bystander autoimmune reactions following the innate immune response.

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