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In addition to the different processes affected by BPs described above, their anti-tumour effect may also involve other elements of the tumour microenvironment - for example, inhibition of proteolytic enzymes required for tumour cell migration, and modification of the capacity of bone marrow precursor cells to migrate to peripheral tissues.
These cells migrate to peripheral tissues and serve as immune sentinels controlling the cytokine landscape.
MCs originate from bone marrow hematopoietic CD34+ progenitor cells, which enter the circulation and migrate to peripheral tissues where they ultimately reside.
Hence, the authors further speculated that CCR7-expressing immature DCs that ingested apoptotic material may migrate to peripheral lymph nodes, in order to maintain tolerance [26].
A requirement for DC function is their ability to migrate to peripheral lymph nodes, where they undertake a key role during the priming of naive T lymphocytes.
CD4+ or CD8+ SP T cells migrate to peripheral tissues, e.g. spleen and peripheral blood, where they are maintained as naïve T cells [1].
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However aside from the gut, it is currently unclear how ILCs may migrate to other peripheral tissues.
These cells migrate to the peripheral immune organs, spleen and lymph nodes.
Thus, stem/progenitor cells migrate to the peripheral circulation following SDF-1α gradients.
They originate in the bone marrow then move into the bloodstream and migrate to the peripheral tissues.
Bone marrow derived EPCs have the capacity to migrate to the peripheral circulation and differentiate into mature endothelial cells [ 24, 25].
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