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Expansion of activated regulatory T cells by myeloid-specific chemokines via an alternative pathway in CSF of bacterial meningitis patients.
|Title||Expansion of activated regulatory T cells by myeloid-specific chemokines via an alternative pathway in CSF of bacterial meningitis patients.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Shi G, Han J, Liu G, Hao Y, Ma Y, Li T, Wu X, Zhang H, Liu Y, Wang B, Kong Y, Zhou J, Zeng H|
|Journal||European journal of immunology|
|Date Published||2013 Oct 23|
Previous studies have demonstrated that activation/expansion by certain cytokines as well as recruitment by specific chemokines is involved in enrichment of regulatory T (Treg) cells in local tissues or organs under pathological conditions. Recent evidence indicates that human Treg cells are a heterogeneous population that comprises three distinct subpopulations: CD25(+) CD45RA(+) resting Treg (rTreg) cells, CD25(hi) CD45RA(-) activated Treg (aTreg) cells, which are both suppressive, and CD25(+) CD45RA(-) cytokine-secreting T cells with proinflammatory capacity. Moreover, rTreg cells can proliferate and convert to aTreg cells. Here, we found an increase in aTreg-cell frequency in the cerebrospinal fluid (CSF) of patients with postneurosurgery bacterial meningitis. We revealed that such an increased aTreg-cell frequency in the CSF was not due to enhanced chemotaxis. Instead of a classic conversion pathway from rTreg to aTreg cells, we identified an alternative route of Treg-cell conversion from cytokine-secreting cells to aTreg cells induced by myeloid-specific chemokine CXC chemokine receptor (CXCR) ligand 5 via CXCR1 and CXCR2 receptors, or by CSF myeloid cells in a cell-cell contact manner. Our results reveal a different view of how the immune system controls overwhelming local immune responses during infection, and provide evidence of how innate immunity negatively regulates adaptive immunity.
|Alternate Journal||Eur. J. Immunol.|