Hematology (Amsterdam, Netherlands) · 2015
Expression of CD154 (CD40L) on stimulated T lymphocytes in patients with idopathic thrombocytopenic purpura.
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Song Ikchan, Kim Jimyung, Kwon Kyechul, Koo Sunhoe, Jo Dukyeon
Аннотация
OBJECTIVES: The role of CD40-CD154 (CD40L) interaction in T cell-dependent humoral immune response is strongly established. Increased expression of CD154 on stimulated T cells is observed in rheumatic diseases and is associated with disease activity. We investigated the expression of CD154 on T cells from idiopathic thrombocytopenic purpura (ITP) patients and assessed the significance of CD154 expression in disease status.
METHODS: We enrolled 59 ITP patients, 23 healthy controls, and 19 patients with non-immune thrombocytopenia. Isolated mononuclear cells were stimulated in RPMI medium containing phorbol myristate acetate (PMA) (5 ng/mL) and ionomycin (500 ng/mL) for 2 h at 37°C. The expression of CD154 on CD4(+)T cells was evaluated using flow cytometry and serum soluble CD40L levels were measured.
RESULTS: In ITP patients, the percentage of CD4(+) CD154(+) cells and mean fluorescence intensity (MFI) of CD154 on activated CD4(+)T cells was not different from that in the healthy controls and non-immune thrombocytopenia patients. Additionally, the percentage and expression level of CD154 was not different between ITP patients with low platelet counts (<50 000/μL) and those with 50 000/μL or more. Soluble CD40L levels were significantly lower in ITP patients with low platelet counts than in healthy controls, but were not correlated with CD154 expression.
CONCLUSION: Increased CD154 expression on CD4(+)T cells was not observed in ITP patients and was not related with low platelet counts. Overexpression of CD154 on CD4(+)T cells is unlikely to be central to the pathogenesis of ITP, and other immune dysfunctions should be targeted for therapy purposes.
METHODS: We enrolled 59 ITP patients, 23 healthy controls, and 19 patients with non-immune thrombocytopenia. Isolated mononuclear cells were stimulated in RPMI medium containing phorbol myristate acetate (PMA) (5 ng/mL) and ionomycin (500 ng/mL) for 2 h at 37°C. The expression of CD154 on CD4(+)T cells was evaluated using flow cytometry and serum soluble CD40L levels were measured.
RESULTS: In ITP patients, the percentage of CD4(+) CD154(+) cells and mean fluorescence intensity (MFI) of CD154 on activated CD4(+)T cells was not different from that in the healthy controls and non-immune thrombocytopenia patients. Additionally, the percentage and expression level of CD154 was not different between ITP patients with low platelet counts (<50 000/μL) and those with 50 000/μL or more. Soluble CD40L levels were significantly lower in ITP patients with low platelet counts than in healthy controls, but were not correlated with CD154 expression.
CONCLUSION: Increased CD154 expression on CD4(+)T cells was not observed in ITP patients and was not related with low platelet counts. Overexpression of CD154 on CD4(+)T cells is unlikely to be central to the pathogenesis of ITP, and other immune dysfunctions should be targeted for therapy purposes.