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Activated murine Treg are CD103+ and can migrate to inflamed tissues.
In some autoimmune diseases, B cells migrate to inflamed sites, where they act as local effector cells [ 2, 3].
ROS production, mediated by high expression of NADPH oxidase, is of critical importance to innate immune cells such as granulocytes, which migrate to inflamed areas and utilize ROS as a defense mechanism against pathogens.
The inflammatory role of circulating monocytes has been related to their ability to migrate to inflamed tissues, to provide effector functions such as cytokine and chemokine production, to undertake phagocytosis and oxidative radical generation, and to their ability to differentiate into different effector cells such as osteoclasts and dendritic cells [ 6, 7].
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In comparison, the frequency of these cells in PB may be less than in healthy control subjects [ 42], presumably because the cells have migrated to inflamed joints.
Memory B cells migrate selectively to inflamed tissues [ 26, 27].
It was shown that Th17 cells express CCR6, which enables them to migrate inflamed tissue in response to CCL20.
Fractalkine (CX3CL1) promotes migration and adhesion of lymphocytes and monocytes to inflamed tissues.
PMNs are the major leukocytes recruited to inflamed sites in response to infection.
Nevertheless, it still blocks neutrophil recruitment to inflamed tissues [ 13].
Therefore, platelets bound to inflammatory cells play a crucial role in recruiting them to inflamed tissues.
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