Journal
NATURE MEDICINE
Volume 24, Issue 7, Pages 1005-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41591-018-0070-2
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Funding
- Pfizer
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Interleukin-2 (IL-2) has been shown to suppress immune pathologies by preferentially expanding regulatory T cells (T-regs). However, this therapy has been limited by off-target complications due to pathogenic cell expansion. Recent efforts have been focused on developing a more selective IL-2. It is well documented that certain anti-mouse IL-2 antibodies induce conformational changes that result in selective targeting of T-regs. We report the generation of a fully human anti-IL-2 antibody, F5111.2, that stabilizes IL-2 in a conformation that results in the preferential STAT5 phosphorylation of T-regs in vitro and selective expansion of T-regs in vivo. When complexed with human IL-2, F5111.2 induced remission of type 1 diabetes in the NOD mouse model, reduced disease severity in a model of experimental autoimmune encephalomyelitis and protected mice against xenogeneic graft-versus-host disease. These results suggest that IL-2-F5111.2 may provide an immunotherapy to treat autoimmune diseases and graft-versus-host disease.
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