New ICG article published in Science Translational Medicine on host-derived mannose glycans as triggers of γδ T cell/IL-17a axis in autoimmunity

Life-threatening autoimmune diseases, including systemic lupus erythematosus (SLE), lead to increasing disability over time, but the underlying mechanisms remain elusive. Now, a new study led by our group has shed light on the role of protein glycosylation in triggering autoreactive immune responses. Our researchers discovered that microbial-associated mannose structures on the kidney’s surface activate DC-SIGN-expressing γδ T cells, leading to a pathogenic interleukin-17a (IL-17a)-mediated autoimmune response. Additionally, we showed that mice lacking Mgat5, which has an abundance of mannose structures, spontaneously developed lupus as they aged. Encouragingly, N-acetylglucosamine supplementation inhibited γδ T cell infiltration and controlled disease development, offering a potential therapeutic strategy for treating autoimmune diseases. This work marks a significant step forward in understanding and potentially treating these debilitating conditions.

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