Abstract: Interleukin-22 (IL-22)is a member of IL-10 cytokine family, and its biological activity is initiated by binding to a cell surface complex composed IL-22R1 and IL-10R2 receptor chains. IL-22 is expressed by most notably T-helper 22 (Th22),Th17 and Th1 cells, partly γδT cells, natural killer cells (NK cells) and lymphoid tissue inducer cells (LTi-like cells). Both of the concentration of IL-22 in tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE) were increased. CD4⁺T cells recruitment from peripheral blood which induced by chemokine/CCR interaction and the differentiation of Th22 cells promoted by IL-1b, IL-6 or tumor necrosis factor-α(TNF-α) from native CD4⁺T cells contribute to the increase. IL-22 was involved in the immunopathology by promoting the expression of matrix metalloproteinases (MMPs) in pleural cavity, and IL-22 could mediate NK cells to produce soluble factors to reduce bacillary growth in M. tuberculosis infected monocyte-derived macrophages. In MPE pleural Th22 cells might be involved in the proliferation and migration of cancer cells,and promote intercellular adhesion of cancer cells to pleural mesothelial cells（PMCs） by upregulating the expression of cellular adhesion molecules. To explore the mechanism of IL-22 in these two diseases will provide new methods for immunodiagnosis and immunotherapy.

Key words: Interleukins, Tuberculosis,pleural, Pleural effusion, malignant