IL17A and tuberculosis: Studies investigating the role of IL-17 in this enhanced pathology have found that increased tissue necrosis and neutrophilic infiltration is dependent on IL-23 and could be ablated by the delivery of anti-IL-17 antibody, suggesting that lung inflammation developing in response to chronic tuberculosis exposure depends on IL-23 and IL-17 (Darrah et al., 2007; Cooper, 2009).