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Harding JS
; Rayasam A
; Schreiber HA
; Fabry Z
; Sandor M
Sci Rep
2015[Oct]; 5
(?): 15248
PMID26515292
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The disappearance and reformation of granulomas during tuberculosis has been
described using PET/CT/X-ray in both human clinical settings and animal models,
but the mechanisms of granuloma reformation during active disease remains
unclear. Granulomas can recruit inflammatory dendritic cells (iDCs) that can
regulate local T-cell responses and can carry bacteria into the lymph nodes,
which is crucial for generating systemic T-cell responses against mycobacteria.
Here, we report that a subset of mycobacterium-infected iDCs are associated with
bacteria-specific T-cells in infected tissue, outside the granuloma, and that
this results in the formation of new and/or larger multi-focal lesions.
Mycobacterium-infected iDCs express less CCR7 and migrate less efficiently
compared to the non-infected iDCs, which may support T-cell capture in
granulomatous tissue. Capture may reduce antigen availability in the lymph node,
thereby decreasing systemic priming, resulting in a possible regulatory loop
between systemic T-cell responses and granuloma reformation. T-cell/infected iDCs
clusters outside the granuloma can be detected during the acute and chronic phase
of BCG and Mtb infection. Our studies suggest a direct role for inflammatory
dendritic cells in the dissemination of granulomatous inflammation.
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