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. 2021 Aug 20;218(10):e20200464. doi: 10.1084/jem.20200464

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© 2021 Lindsay et al.

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Figure 6. — MERTK signaling drives suppression of antigen-dependent T cell–APC interactions in islets. Activated 8.3 CD8 T cells (white), BDC-2.5 CD4 T cells (red), and polyclonal T cells (blue) were fluorescently labeled and cotransferred into female NOD.CD11c-YFP mice (green). Mice were treated twice daily with saline vehicle or 30 mg/kg UNC2025. 17 h following the initial treatment, islets were isolated and analyzed by two-photon microscopy. (A) Schematic of experimental setup. (B) Average level of islet infiltration. (C) Representative islet images from vehicle- or UNC2025-treated mice with 5-min tracks of motion. White and gray arrows point to sustained interactions between 8.3 T cells and CD11c cells. Red arrows point to sustained interactions between BDC-2.5 T cells and CD11c cells. (D) Percentage of T cells participating in sustained interactions (≥10 min) with CD11c⁺ cells. Scale bars, 10 µm. (E) Average duration of interaction between T cells and CD11c⁺ cells. (A–E) n = 16–17 islets from vehicle-treated mice containing 575 analyzed BDC-2.5 T cells, 168 analyzed 8.3 T cells, and 470 analyzed polyclonal T cells. n = 8–9 islets from UNC2025 treated mice containing 356 analyzed BDC-2.5 T cells, 60 analyzed 8.3 T cells, and 907 analyzed polyclonal T cells. Data were derived from two or three independent experiments. (B, D, and E) Statistics: two-tailed Student’s t test; *, P < 0.05; ****, P < 0.0001. Error bars represent SEM.