Vietnam has achieved WHO's leprosy elimination goal at a national level, but there are a lot of ex-leprosy patients who have severe physical disabilities in the leprosy treatment centers and resettlement villages.
  The purpose of this study is to analyze the quality of life (QOL) of ex-leprosy patients in Vietnam.
  The study was conducted in two leprosy treatment centers in Vietnam. The SF-36v2 QOL survey was used to evaluate the leprosy patients' health related conditions, and as a comparison group, SF-36v2 QOL survey was provided to a random group from the general population to measure the general groups' health related conditions.
  For those participants aged from 10 to 29 years old, the patients' group scored lower than the general group in each of the following categories; Role physical, Bodily pain, General health perceptions, Vitality, Social functioning, Role emotional.
  On the other hand, middle aged and elderly participants were found to show no significant difference between the patients' group and the general group. In comparing the two leprosy treatment centers, the score of Role physical and Role emotional were significantly higher in the leprosy treatment center where vocational training programs for leprosy patients are offered. From these results, the use of vocational training program is one of the effective methods for improving the QOL of the patients' group.

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  The objectives of this paper are to grasp the current status of an endemic disease, known as Buruli ulcer (BU), in the Republic of Togo and the expansion of international assistance in the field. By adopting the explicit support model, this paper also compares the obtained research results with those of the Republic of Ghana and Benin, to clarify the primary functions played among respective governments, WHO, and NGO.
  Under the auspices of the WHO Global Buruli Ulcer Initiative (GBUI, 1998−), National Buruli Ulcer Control Programme (NBUCP) in the Togo was initiated in 1999. However, due to the shortage of national budget and politico-economic instabilities of the nation, the actual implementation of NBUCP proved to be problematic. It was after 2007 that the programme began to move forward with the interventions of NGOs like DAHW and Handicap International.
  Currently, major players involved in the implementation of the policies provided by the GBUI are WHO, NGOs and the targeted governments. In other words, the organizations involved in BU treatment work together by fulfilling their functions. Unlike the neighboring countries, the Togolese government encountered much difficulty in materializing its national programme. Largely due to the political instability and the severe shortage of national budget, stronger assistances from NGOs were required at various levels of the national health measures from formulating to implementing the programme. As the programmes in Togo and Ghana/Benin expanded over the years, the respective support model revealed to be unique and different. In Ghana and Benin, intimate cooperation among WHO, government and NGOs has been established. In Togo, strengthening of collaboration among the three players is expected.

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  A novel recombinant BCG (BCG-DHTM), that was deficient in urease, expressed with gene encoding the fusion of BCG-derived HSP70 and M. tuberculosis-derived major membrane protein (MMP)-Ⅱ, was constructed for use as a vaccine against tuberculosis. BCG-DHTM efficiently activated dendritic cells (DC) to induce cytokine production, including IL-12, TNFα and IL-1β and phenotypic changes. The DC infected BCG-DHTM was more potent in activation of naïve T cells of CD4 and CD8 subsets than those infected vector control BCG. The activation of naïve T cells by BCG-DHTM was closely associated with phagomal maturation, and that of naïve CD8⁺ T cells by BCG-DHTM was induced by the activation of cytosolic cross-presentation pathway. Further, BCG-DHTM seemed to activate naïve CD4⁺ T cells and naïve CD8⁺ T cells by antigen-specific fashion. The primary infection of BCG-DHTM in C57BL/6 mice for 12 weeks efficiently produced T cells responsive to in vitro secondary stimulation with MMP-Ⅱ HSP70 and H37Rv-derived cytosolic protein and inhibited with multiplication of subsequently challenged M. tuberculosis in lungs at least partially.
  The effect of BCG-DHTM as a vaccine for tuberculosis is not fully convincing and need the improvement, however, our strategy in the development of new recombinant BCG for tuberculosis seems to provide useful tool.

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  The effectiveness of a vaccine against tuberculosis and leprosy is mainly judged by its capability to induce memory CD8⁺ cytotoxic T cells (CTL). It has been reported that ‘help’ from CD4⁺ T cells is required to induce memory CTL.
   However, how CD4⁺ T cells instruct or support memory CTL during priming phase has not been resolved in detail. Therefore, we examined the helper function of CD4⁺ T cells in CTL differentiation.
  Peptide-25 is the major T cell epitope of Ag85B of Mycobacterium tuberculosis. We found that this peptide induced the expression of T-bet and TATA box binding protein-associated factor that can induce the chromatin remodeling of ifn-γ gene, and as a result induced Th1 differentiation even in the absence of IFN-γ and IL-12. Next, we established an in vitro CTL differentiation system using Peptide-25, Peptide-25 specific CD4⁺ T cells, OVA specific CD8⁺ T cells and splenic DC. By using this system, we found that CD4⁺ T cells activated DC even in the absence of IFN-γ and CD40 ligand association, and the activated DC induced the functional differentiation of CTL. To identify the regulatory factors for DC activation, we analyzed the gene expression profile of helper CD4⁺ T cells and identified 27 genes.
  Taken together, these results suggest that the inducing factors for Th1 differentiation are not indispensable to induce the functional differentiation of CTL.

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  Instead of rapid multiplication, pathogenic mycobacteria, such as Mycobacterium tuberculosis are likely to have acquired slow but long life. Host immunity affords desirable non-competitive environment for M. tuberculosis in human lungs, where this pathogen slowly grows or arrests growing, which avoids rapid loss of living places. Mycobacterial DNA-binding protein 1 (MDP1), a unique histone-like protein associating mycobacterial GC-rich DNA, has pivotal role in realizing such slow life and pathogenesis including drug tolerance to isoniazid.

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  Pulmonary tuberculosis is an infectious disease caused by Mycobacterium tuberculosis, and continues to be a serious threat to human life. Since M. tuberculosis establishes intracellular parasitism in macrophages, host innate and acquired immune systems have to detect and enhance bactericidal activity against the intracellular bacteria. Understanding of interaction between pathogenic factors of M. tuberculosis and host is also important to understand how immune system copes with the pathogen. In this review, we shortly summarize the mechanisms how innate and acquired immunity recognize M. tuberculosis or M. tuberculosis-infected cells and protects hosts from the infection. Furthermore, IL-17A/IL-23 axis, a recently focused inflammatory cytokine system, is discussed in the context of anti-mycobacterial protective immunity.

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[in Japanese]

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  ad hoc committee of Japanese Leprosy Association recommends revised standard treatment protocol of leprosy in Japan, which is a modification of World Health Organization's multidrug therapy (WHO/MDT, 2010). For paucibacillary (PB) leprosy, 6 months treatment by rifampicin and dapsone (MDT/PB) is enough. However, for high bacterial load multibacillary (MB) leprosy, 12 months treatment seems insufficient. Thus, (A) For MB with bacterial index (BI) > 3 before treatment, 2 years treatment by rifampicin, dapsone and clofazimine (MDT/MB) is necessary. When BI becomes negative and active lesion is lost within 2 years, no maintenance therapy is necessary. When BI is still positive, one year of MDT/MB is added (3 years in total), followed by maintenance therapy by dapsone and clofazimine until BI negativity and loss of active lesions. (B) For MB with BI < 3 or fresh MB (less than 6 months after the onset of the disease) with BI > 3, 1 year treatment by MDT/MB is necessary. When BI becomes negative and active lesion is lost within one year, no maintenance therapy is necessary. When BI is still positive or active lesion is remaining, additional therapy with MDT/MB for one more year is recommended. Brief summary of diagnosis, purpose of therapy, character of drugs, and prevention of deformity is also described.

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