Production of TNF-α was inhibited in the patient’s serum, whereas IL-10 production was not (Fig. 2C and D). Disseminated NTM disease usually occurs in patients who are severely immunocompromised, such as those with HIV disease or AIDS. However, some dNTM disease cases do not have HIV infection. There are two retrospective clinical analyses of dNTM disease without HIV infection.7 and 8 Chou et al. reported that

their 18 patients without HIV infection were usually febrile with elevated WBC counts.7 NTM was mainly isolated from not only the lung but also blood or bone marrow, and MAC was the most frequently detected pathogen in their study.7 Chetchotisakd et al. reported that NTM was selleck chemical most frequently detected in lymph nodes in their 129 dNTM patients without HIV infection.8 It is noteworthy that in both of these studies, dNTM patients had other opportunistic or severe infections in addition to the NTM. These included Salmonellosis, severe systemic intravascular PF-02341066 purchase infection, fungal infections including Aspergillus spp, Candida spp and Penicillium marneffei,

and viral infections including varicella zoster and cytomegalovirus. Furthermore, the cases with dNTM disease, confirmed by detection of NTM in multiple specimens, often did not have HIV. With adequate anti-AFB treatment, the survival rate was better than without such treatment. Female gender and co-infection with other bacterial pathogens were associated with poor outcomes. However, HIV infection had no significant prognostic impact. In 2005, two important studies detected autoantibodies against IFN-γ

in plasma from dNTM patients without HIV L-NAME HCl infection.4 and 5 IFN-γ has a crucial role in the control and regulation of NTM disease because some mutations in the genes for Th1 cytokines and their receptors are associated with severe conditions.9 Watanabe et al. reported that anti-IFN-γ autoantibody is detected even in sera from healthy individuals.10 However, the reason for the existence of an autoantibody against IFN-γ remains unclear. Evaluating anti-IFN-γ autoantibody in healthy individuals is important for elucidating the autoantibody differences between dNTM patients and healthy individuals. There must be an underlying factor triggering the onset of dNTM disease in the absence of HIV-infection. Regarding these previous reports, we considered it to be important for understanding the present patient’s pathophysiology to assay his serum. We wanted to know whether his serum contained specific immunoglobulins which bound and neutralized IFN-γ. To assay anti-IFN-γ autoantibody, we applied a protocol allowing comparison with bioassay results obtained using normal PBMNCs, as described in previous reports.5 In our view, mediastinal lymphadenopathy with elevated WBC counts and leukocytosis, of unknown origin, should prompt assay of the patient’s serum to detect anti-IFN-γ autoantibody. In addition, we suggest that infectious organisms such as P.