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Biology subjects

St. Jean, S.

Publications and source records attributed to St. Jean, S..

2 recordsLinked to original sources

Systemic Autoimmunity Remodels Microbiota-Reactive CD4⁺ T Cell Immunity

The gut microbiota contributes to autoimmune disease, yet how systemic autoimmunity reshapes microbiota-reactive CD4 T cell responses and how these cells influence disease progression remain poorly understood. Previous studies have linked microbiota-reactive T cells and lupus-associated pathobionts to disease pathogenesis, but the pathways that regulate the accumulation, differentiation, and pathogenicity of microbiota-reactive T cells during autoimmunity remain unclear. Here, we show that systemic autoimmunity drives the expansion, accumulation, and functional differentiation of microbiota-reactive CD4 T cells. Using segmented filamentous bacteria tetramers, we identify antigen-defined microbiota-reactive CD4 T cells that undergo systemic accumulation and Th1/Tfh polarization during disease. We further identify reactivation of intestinal dendritic cell trafficking as a mechanism linking systemic autoimmunity to the accumulation of microbiota-reactive CD4 T cells in peripheral tissues. In contrast to commensal-reactive T cells, CD4 T cells conditioned by the lupus-associated pathobiont Enterococcus gallinarum markedly exacerbate autoimmunity following adoptive transfer through IL-21- and IFN{gamma}-dependent mechanisms. Together, these findings demonstrate that systemic autoimmunity reshapes microbiota-reactive CD4 T cell immunity and establish microbial context as a critical determinant of microbiota-reactive CD4 T cell pathogenicity.

immunology↗

Tissues Guide Dependence of Treg on the Transferrin Receptor

Activated T cells increase transferrin-bound iron uptake via the transferrin receptor, also called CD71. We previously demonstrated that targeting CD71 with an antibody to reduce iron update can modify CD4 T cell function, with different effects on TH1, TH17, and regulatory T (Treg) cells. CD71 blocking antibody-treated Tregs had no loss of viability or differentiation, and Foxp3 expression was increased. However, a genetic deletion of Tfrc (the gene for CD71) driven by Foxp3-Cre was reported to cause a lethal autoimmunity. Whether altered immune homeostasis or insufficient early developmental tolerance drive the phenotype of CD71 knockout (KO) Treg mice were unclear. Here, we examined the Foxp3-YFP-Cre KO mouse model and a tamoxifen-inducible KO model in adults to determine the role of CD71 expression in Treg cells. We hypothesized that due to a lack of iron for mitochondrial metabolism, KO Treg adapt to rely heavily on glycolysis and become unstable, promoting pro-inflammatory exTreg cells. This effect was not universal, however, and necropsy analyses revealed tissue-specific inflammation. While the colons of mice with KO Treg cells appeared healthy, skin and lung tissue were severely inflamed. Metabolically, KO Treg cells had a significant decrease in their glycolytic capacity and instead increased oxidation of amino acids and fatty acids. In inflamed skin, which that promotes increased oxidative stress, CD71 expression in Treg cells suppressed tissue inflammation in a model of atopic dermatitis-like disease. These results indicate the CD71-iron axis as a new immunometabolic regulator of Treg cell functions in immune and non-immune organs. Capsule SummaryA loss of the transferrin receptor in Tregs causes severe autoimmunity and here we clarify how Tregs rely on this receptor for iron in specific tissues and disease settings including atopic dermatitis.

immunology↗