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In HIV/SIV infections, for example, pDCs migrate to lymphoid organs or mucosal tissues and contribute to pathological changes in these areas (Nascimbeni et al. 2009; Kwa et al. 2011; Li et al. 2013).
Finally they migrate to lymphoid organs in order to present processed antigens to lymphocytes and to stimulate immune responses [2].
Only upon receiving maturation signals, DCs migrate to lymphoid organs, secrete cytokines and express co-stimulatory molecules that are required for lymphocyte activation [1].
In our study we show that contact-dependent induced regulatory DCs up-regulate the expression of CCR7 thereby enabling these DCs to migrate to lymphoid tissues where they may induce tolerance.
With increased expression of CCR7 and CD62L, central memory T cells are programmed to preferentially migrate to lymphoid tissues to interact with other T and B cells in establishing a repertoire of effector functions against the invading pathogen [26].
Acute GvHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after allogeneic stem cell transplantation.
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Finally, Tregs could have migrated to lymphoid tissues, as suggested by previous studies in humans and macaques [17], [18], [42].
Once the cells have migrated to lymphoid organs, PGE2 assumes a suppressive action, inhibiting the maturation of DC and their ability to present antigen [19]" [19].
Intratumorally injected DCs would acquire and process tumour antigens in situ, migrate to regional lymphoid organs via lymphoid vessels, and initiate a significant tumour-specific immune response.
When these DCs are activated by antigens and mature, they migrate from peripheral sites to lymphoid organs where they stimulate T cells to induce an immune response [11], [30].
Due to the lack of intra-CNS lymphatic vessels, the question whether and how DCs migrate from the inflamed CNS to lymphoid organs is still controversial.
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