Cancer immune evasion following treatment is a major issue for immunotherapies such as immune checkpoint blockade (ICB), whereby adaptive resistance to treatment can occur following an initial response, leading to poor prognosis.Previous work has found that downregulation of CD58, the co-stimulatory ligand for CD2, is associated with immune evasion in melanoma tumours and that ICB treatment of renal cell carcinoma is associated with decreased CD58 expression. However, the mechanism is poorly understood. In this preprint (not peer-reviewed), Ho et al. investigated both the role of CD58 expression in cancer cell immune evasion and the protein interactions of CD58.
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