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Here we show that treatment of mice with a non-cytotoxic heavy-chain antibody that selectively inhibits CD38 ectoenzyme resulted in NAD + boosting that was associated with significant protection from fibrosis in multiple organs

Csardi, G

Taken together, the pattern suggests that a controlled, short-lived immune activation may accompany epithelial repair, consistent with the accelerated wound closure observed in HCEpiC assays under basal, inflammatory and oxidative stress conditions ( Importantly, the interpretation of increased Th1-associated cytokines as part of a repair-associated response rather than purely deleterious inflammation is supported by emerging evidence on corneal wound healing biology (Wilson, 2020)