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Mycobacterium tuberculosis PstS1 amplifies IFN-gamma and induces IL-17/IL-22 responses by unrelated memory CD4(+) T cells via dendritic cell activation
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2013 (English)In: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 43, no 9, 2386-2397 p.Article in journal (Refereed) Published
Abstract [en]

The immunological mechanisms that modulate protection during Mycobacterium tuberculosis (Mtb) infection or vaccination are not fully understood. Secretion of IFN- and, to a lesser extent, of IL-17 by CD4(+) T cells plays a major role both in protection and immunopathology. Few MtbAgs interacting with DCs affect priming, activation, and regulation of Ag-unrelated CD4(+) T-cell responses. Here we demonstrate that PstS1, a 38 kDa-lipoprotein of Mtb, promotes Ag-independent activation of memory T lymphocytes specific for Ag85B or Ag85A, two immunodominant protective Ags of Mtb. PstS1 expands CD4(+) and CD8(+) memory T cells, amplifies secretion of IFN- and IL-22 and induces IL-17 production by effector memory cells in an Ag-unrelated manner in vitro and in vivo. These effects were mediated through the stimulation of DCs, particularly of the CD8(-) subtype, which respond to PstS1 by undergoing phenotypic maturation and by secreting IL-6, IL-1 and, to a lower extent, IL-23. IL-6 secretion by PstS1-stimulated DCs was required for IFN-, and to a lesser extent for IL-22 responses by Ag85B-specific memory T cells. These results may open new perspectives for immunotherapeutic strategies to control Th1/Th17 immune responses in Mtb infections and in vaccinations against tuberculosis.

Place, publisher, year, edition, pages
2013. Vol. 43, no 9, 2386-2397 p.
Keyword [en]
DC, Memory T cells, Mycobacterium tuberculosis Ags, Th1 response, Th17 response
National Category
Immunology
Identifiers
URN: urn:nbn:se:su:diva-98324DOI: 10.1002/eji.201243245ISI: 000327819200018OAI: oai:DiVA.org:su-98324DiVA: diva2:683356
Note

AuthorCount:9;

Available from: 2014-01-03 Created: 2014-01-03 Last updated: 2017-12-06Bibliographically approved

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