tuberculosis infection [8]. This importance is underscored by the observation that children with hereditary IFN-γ receptor 1 deficiency are prone to M. tuberculosis infection or to dissemination of BCG after vaccination [9–11]. Furthermore, IFN-γ treatment has shown promising results in patients with multidrug-resistant PTB [12]. IL-22 belongs to the IL-10 family, which signals through a receptor complex see more IL-22R1/IL-10R2 [13–15]. IL-10R2 is highly expressed on immune cells. However, IL-22R1 is specifically expressed on epithelial and some fibroblast

cells in peripheral tissues such as gastrointestinal, respiratory system and skin [16]. IL-22 can induce tissue expression of acute inflammatory proteins, mucins or antimicrobial peptides, which are important for tissues to maintain their integrity during chronic inflammation [17]. IL-17 is found to induce human fibroblasts and bronchial epithelial cells to express IL-8 and G-CSF, triggering recruitment of neutrophils check details to the lung and facilitating granuloma formation [18–20]. IL-17 can also initiate recruitment of Th1 cells to the lung by upregulating CXCL9, CXCL10 and CXCL11, which can eventually control bacterial growth and defence after M. tuberculosis infection

[21]. Patients with tuberculous pleurisy (TBP) have a relatively strong immune response against M. tuberculosis infection [22], and the disease results from delayed hypersensitivity involving macrophages, T cells and cytokines. Therefore, we took TBP as a relevant model to study

the immune inflammatory response at the local site of M. tuberculosis infection. ESAT-6 and CFP-10 are used to test specific responses because these antigens may be critical in the development of protective immunity to M. tuberculosis infection. They are present in all M. tuberculosis and pathogenic Mycobacterium bovis strains but lacking in all BCG strains [23]. Our data demonstrate for the first time that ESAT-6-, CFP-10- and BCG-specific Th1, Th22 and Th17 cells are present at the local site of infection in patients with TBP and these cells may play an important role in the local protective cellular immunity. Subjects.  The study was conducted among 23 patients with TBP: 11 men and 12 women aged 19–83 years (mean = 39.82 years). All Adenylyl cyclase participants were from the Chest Hospital of Guangzhou, and they had written informed consent. The diagnosis of tubercular pleural effusion was made on the basis of the following criteria: medical history, physical examination, chest X-ray, isolation of M. tuberculosis from the pleural fluid or tissue, a smear positive for acid-fast bacilli from the pleural fluid or tissue or a positive mycobacterium culture. None of the patients was on anti-TB treatment at the time of enrolment in the study. Exclusion criteria included positive HIV test or the presence of concurrent infectious diseases. Pleural fluid samples were obtained during therapeutic thoracentesis.