Data S3. Effects of CatG addition on MHC II levels in intact APC (Western blot). Data

S4. Effects of CatG addition on cell surface MHC II levels in intact APC. Data S5. Effects of CatG inhibition on cell surface MHC II levels using primary intact APC. Please note: Wiley-Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“The problems of tuberculosis (TB) and its drug resistances are very severe in China. New therapeutic agents or regimens to treat multi-drug-resistant tuberculosis (MDR-TB) CX-5461 are urgently needed. We studied the effects of Ag85A DNA vaccine alone or in combination with rifampin

(RFP) or pyrazinamide (PZA) for the treatment of MDR-TB in mice. Ag85A DNA vaccine significantly increased the production of IFN-γ, but lowered the production of IL-4. Seventy female BALB/c mice infected with Mycobacterium tuberculosis clinical isolate HB361, which was resistant to RFP and isoniazid but sensitive to PZA, were treated with plasmid pVAX1, RFP, PZA, M. vaccae vaccine, Ag85A DNA, Ag85A DNA combined with RFP or PZA, respectively. Ag85A DNA vaccine alone or in combination with RFP or PZA reduced the pulmonary and splenic bacterial loads by 1.03–1.38 logs, respectively. Ag85A DNA combined with conventional chemotherapy for the treatment of MDR-TB might result in cure of MDR-TB in developing countries. Tuberculosis (TB) selleckchem accounts for four deaths every minute and two million annual deaths [1]. It remains the most widely spreading infectious disease and a leading cause of death throughout the world. Multi-drug-resistant SPTLC1 tuberculosis (MDR-TB) has emerged as a new challenge, especially in developing countries. This is mainly because of the lack of funding to support the treatment of MDR-TB with second line anti-tuberculosis drugs [2]. Southeast Asia and Western Pacific regions account for almost 60% of the newly occurring MDR-TB cases globally [3]. DNA vaccination has been pursued for the treatment of tuberculosis (TB) because it establishes cellular immune responses, including T helper (Th) 1 immune

responses and cytotoxic T lymphocyte. Th1 immune responses drive the induction of cellular immunity, whereas Th2 immune responses preferentially drive humoral immunity. The Th1-type cytokine interferon (IFN)-γ is essential for the control of TB in mice and is the first human immunologic factor essential for resistance against mycobacterial infection [4, 5]. Functional analysis of genes suggested that DNA 65-kDa heat-shock protein (hsp65) therapy not only boosts the Th1 immune response, but also inhibits Th2 cytokines and regulates the intensity of inflammation through fine tuning of gene expression of various genes, including interleukin-17, lymphotoxin A, tumour necrosis factor-alpha, interleukin-6, transforming growth factor-beta, inducible nitric oxide synthase and Foxp3 [6].