Figure 6.

Proposed role of BTNL8 in MIS-C. Schematic diagram of proposed mechanism of BTNL8 contribution to MIS-C. Upon infection with SARS-CoV-2, BTNL8 variants are unable to effectively engage with Vγ4+γδ T cells contributing to underlying intestinal inflammation subsequently leading to a hyperinflammatory state. Image created with https://BioRender.com.

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