This suggests that pro-IL-1α could be released during tissue damage where it acts weakly as a DAMP, however, if there is sufficient damage or infection for recruitment of immune cells, which produce granzyme B (cytotoxic B-cells and T-cells), neutrophil elastase (neutrophils) and chymase (basophils and mast cells), the proinflammatory IL-1α signal will be amplified through pro-IL-1α cleavage into more active forms70,71. Here, CMA1 is linked to infection.