Three major points emerged: (1) IL-17 was not abundant at sites of TB disease, and expression of IL-17 by PPD-specific CD4 T cells from disease sites was not detected, (2) IL-22 was readily detected in pleural and pericardial effusions at levels exceeding those detected in matching peripheral blood, and (3) levels of pericardial IL-22 correlated with MMP-9 levels in pericardial fluid and peripheral blood, suggesting a role for IL-22 in TB induced pathology. This evidence concerns the gene IL22 and tuberculosis.