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Helminth Infections Coincident with Active Pulmonary Tuberculosis Inhibit Mono- and Multifunctional CD4 and CD8 T Cell Responses in a Process Dependent on IL-10
While it has long been recognized that helminth infections alter the pathophysiology of allergic and autoimmune disease, data suggest that helminth infections also exert an important immunological effect on concomitant infections and vaccine responses. In particular, helminth coinfection can modulate the severity, pathogenesis and transmission of other infectious diseases. In this study, we examine the mechanism by which helminth infections modulate the immunological responses to tuberculosis antigens in individuals with active pulmonary tuberculosis. Our data suggest that two different helminth infections, with different life cycles, tissue localization and modes of transmission essentially exert very similar effects on the adaptive immune response to tuberculosis antigens in pulmonary tuberculosis. This includes a compromised induction of protective cytokine-expressing T cells as well as inhibitory effects on systemic cytokines that are potentially protective in tuberculosis. The strength of this study lies in the fact that this is the first study to demonstrate that two different helminth infections essentially impair cytokine responses in a similar manner in pulmonary tuberculosis.
Vyšlo v časopise: Helminth Infections Coincident with Active Pulmonary Tuberculosis Inhibit Mono- and Multifunctional CD4 and CD8 T Cell Responses in a Process Dependent on IL-10. PLoS Pathog 10(9): e32767. doi:10.1371/journal.ppat.1004375
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004375Souhrn
While it has long been recognized that helminth infections alter the pathophysiology of allergic and autoimmune disease, data suggest that helminth infections also exert an important immunological effect on concomitant infections and vaccine responses. In particular, helminth coinfection can modulate the severity, pathogenesis and transmission of other infectious diseases. In this study, we examine the mechanism by which helminth infections modulate the immunological responses to tuberculosis antigens in individuals with active pulmonary tuberculosis. Our data suggest that two different helminth infections, with different life cycles, tissue localization and modes of transmission essentially exert very similar effects on the adaptive immune response to tuberculosis antigens in pulmonary tuberculosis. This includes a compromised induction of protective cytokine-expressing T cells as well as inhibitory effects on systemic cytokines that are potentially protective in tuberculosis. The strength of this study lies in the fact that this is the first study to demonstrate that two different helminth infections essentially impair cytokine responses in a similar manner in pulmonary tuberculosis.
Zdroje
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