Mycobacterium avium Subspecies paratuberculosis Drives an Innate Th17-Like T Cell Response Regardless of the Presence of Antigen-Presenting Cells.

摘要: The gastrointestinal disease of ruminants is clinically known as Johne's (JD) and caused by Mycobacterium avium subspecies paratuberculosis (MAP). An accumulative effect insensitive diagnostic tools, a long subclinical stage infection, lack effective vaccines have made the control JD difficult. Currently lacking in model systems are undefined correlates protection sources inflammation due to JD. As an alternative commonly studied immune responses, such Th1/Th2 paradigm, non-classical Th17 response MAP has been suggested. Indeed antigens induce mRNAs encoding Th17-associated cytokines IL-17A, IL-17F, IL-22, IL-23, IL-27, IFNγ CD3+ T cell cultures determined RT-qPCR. Although not robust when cultured with monocyte-derived macrophages (MDMs), able stimulate upregulation these from sorted cells absence antigen-presenting (APCs). CD4+ CD8+ main contributors IL-17A IL-22 APCs. However, MAP-stimulated MDMs contributor IL-23. In vivo, JD+ cows more circulating IL-23 than JD- cows, suggesting that this proinflammatory cytokine may be important etiology Our data study continue suggest Th17-like associated indeed play role responses infection development or