Tuberculous lymphadenitis (TBL) is characterized by an expansion of Th1 and Th17 cells with altered serum levels of proinflammatory cytokines. However, the cytokine profile at the site of infection, i.e., the affected lymph nodes, has not been examined in detail. To estimate the baseline and mycobacterial antigenstimulated concentrations of type 1, type 17, and other proinflammatory cytokines in patients with TBL (n ϭ 14), we examined both the baseline and the antigen-specific concentrations of these cytokines before and after chemotherapy and compared them with those in individuals with pulmonary tuberculosis (PTB) (n ϭ 14). In addition, we also compared the cytokine responses in whole blood and those in the lymph nodes of TBL individuals. We observed significantly enhanced baseline and antigen-specific levels of type 1 cytokines (gamma interferon [IFN-␥] and tumor necrosis factor alpha [TNF-␣]) and a type 17 cytokine ) and significantly diminished baseline and antigen-specific levels of proinflammatory cytokines (IL-1 and IL-18) in the whole blood of TBL individuals compared to those in the whole blood of PTB individuals. Moreover, we also observed a pattern of baseline and antigen-specific cytokine production at the site of infection (lymph node) similar to that in the whole blood of TBL individuals. Following standard antituberculosis (anti-TB) treatment, we observed alterations in the baseline and/or antigen-specific levels of IFN-␥, TNF-␣, IL-1, and IL-18. TBL is therefore characterized by enhanced baseline and antigen-specific production of type 1 and type 17 cytokines and reduced baseline and antigen-specific production of IL-1 and IL-18 at the site of infection.KEYWORDS tuberculosis, lymphadenitis, cytokines I mmune responses in tuberculous lymphadenitis (TBL) are poorly understood, although TBL is the most common form of extrapulmonary TB, accounting for 30 to 40% of cases (1). TBL commonly affects the superficial lymph nodes (LN) of the body, with the cervical lymph nodes being the most commonly affected, followed by the inguinal, axillary, mesenteric, mediastinal, and intramammary lymph nodes (2). The pathogenesis of TBL and/or the pathway of dissemination from the lungs is still unclear,