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Extracorporeal Photopheresis Normalizes Some Lymphocyte Subsets (Including T Regulatory Cells) in Chronic Graft‐Versus‐Host‐Disease
Author(s) -
Bladon John,
Taylor Peter
Publication year - 2008
Publication title -
therapeutic apheresis and dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 53
eISSN - 1744-9987
pISSN - 1744-9979
DOI - 10.1111/j.1744-9987.2008.00593.x
Subject(s) - foxp3 , medicine , il 2 receptor , regulatory t cell , immunology , extracorporeal photopheresis , cd8 , graft versus host disease , photopheresis , immune system , t cell , cytotoxic t cell , transplantation , biology , in vitro , lymphoma , biochemistry
Extracorporeal photopheresis (ECP) has been demonstrated to be clinically effective for the treatment of steroid‐refractory graft‐versus‐host‐disease (GvHD). Recently, a murine model suggested that ECP may modulate the allo‐reactivity, seen in GvHD, by enhancement of T regulatory cells. T regulatory cells are an important component of immune tolerance and reduced levels of them have been observed in chronic GvHD. Samples were taken from eight chronic GvHD patients prior to receiving any ECP therapy and after three months of ECP. Samples were also obtained from eight age‐ and sex‐matched normal controls. Each sample was evaluated for absolute levels of total lymphocytes and CD4 + and CD8 + T cells. T regulatory cell numbers were also assessed accordingly: CD4 + CD25 high , CD4 + CD25 high CD69 ‐ , CD4 + CD25 high CD152 + and CD4 + CD25 high FOXP3 + . Following three months of ECP, increases in the absolute counts of total lymphocytes, CD4 + and CD8 + T cells and T regulatory cells were observed; however, no selective statistical increase in the percentage of T regulatory cell numbers was observed within the CD4 + T cell compartment. ECP induces an increase in T regulatory cell numbers; however, this is not specific as there is also an enhancement of both total lymphocyte and CD4 + T cell numbers. The positive effect of ECP may therefore depend on a more generic re‐adjustment of immune homeostasis.