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Mycobacterium smegmatis infects human monocytes that can be precursors of dendritic cells. We tested whether the interaction of M. smegmatis with monocytes modulated their differentiation into dendritic cells. We found that M. smegmatis-infected monocytes differentiated into CD1a-CCR7+ dendritic cells in the presence of GM-CSF and IL-4 and acquired a mature phenotype since they expressed CD83 molecules in the absence of maturation stimuli. Dendritic cells derived from M. smegmatis-infected monocytes stimulated with bacterial products, produced IL-10 and still retained the capacity to produce IL-12. Consequently, they polarized naïve T lymphocytes towards a mixed Th1/Th2 immune response inducing both IFN-gamma and IL-4 production. These findings suggest that the exposure to environmental mycobacteria could modulate the differentiation of dendritic cells making them able to migrate into secondary lymphoid organs and modulate the adaptive immune response. This could explain one of the mechanisms by which environmental mycobacteria can influence the immune response to pathogenic species.

The association between an acquired form of hyper-IgM syndrome and a chronic hepatitis C virus (HCV) infection in a 71-year-old female patient is described. Both diseases were diagnosed at the age of 58 years. She was started on intramuscular and then intravenous immunoglobulin replacement therapy. HCV RNA was detected in 1992. The patient remained in well-balanced clinical condition until 1994, when total and specific anti-HCV IgM levels increased and the patient developed an IgM kappa monoclonal gammopathy. Adherent cells and B cells were HCV RNA positive, while T cells were HCV RNA negative. Anti-IgM reactivity was specifically directed to the core antigen of the HCV. The patient we describe showed a picture of a late-onset form of hypogammaglobulinemia with a progressive increase in IgM antibodies, possibly due to the concomitant HCV infection. It is possible that the immunodeficiency might also result from the HCV infection, with formation of specific antibodies belonging to the IgM class, and that the worsening of the clinical condition may be directly related to the persistent viral infection.