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RESEARCH PRODUCT
CD4+ CCR5+ and CD4+ CCR3+ lymphocyte subset and monocyte apoptosis in patients with acute visceral leishmaniasis
Serafino MansuetoMarcella PotestioGiuseppina Colonna RomanoSalvatore MilanoGloria Di BellaPietro D'agostinoG. GambinoAlessandra AquinoViviana FerlazzoR. CarusoGiustina VitaleEnrico Cillarisubject
AdultCD4-Positive T-LymphocytesProgrammed cell deathChemokineReceptors CCR5Receptors CCR3ImmunologyAntigens ProtozoanApoptosisCD8-Positive T-LymphocytesBiologyPeripheral blood mononuclear cellMonocytesParacrine signallingAntigenmedicineHumansImmunology and Allergyfas ReceptorAutocrine signallingCells CulturedMonocyteOriginal ArticlesTh1 CellsLymphocyte Subsetsmedicine.anatomical_structureApoptosisAcute DiseaseImmunologyLeukocytes Mononuclearbiology.proteinLeishmaniasis VisceralReceptors Chemokinedescription
The potential involvement of apoptosis in the pathogenesis of visceral leishmaniasis (VL) was examined by studying spontaneous and Leishmania antigen (LAg)-induced apoptosis using cryopreserved peripheral blood mononuclear cells (PBMC) of Sicilian patients with VL. Results indicate that monocytes and T lymphocytes from acute VL patients show a significantly higher level of apoptosis compared with that observed in healed subjects. The percentage of apoptotic cells was higher in monocytes than in T lymphocytes. T cells involved in programmed cell death (PCD) were mainly of the CD4(+) phenotype. In particular, the T helper 1-type (Th1) subset, as evaluated by chemokine receptor-5 (CCR5) expression, is involved in this process. Cell death in Th1-type uses a CD95-mediated mechanism. Furthermore, Th1-type CCR5(+) cells are prone to cell suicide in an autocrine or paracrine way, as attested by enhanced expression of CD95L in acute VL patients. The reduction in Th1-type cells by apoptosis was confirmed by the decrease in interferon-gamma secretion. In conclusion, apoptosis of monocytes, CD4(+) and CD4(+) CCR5(+) T cells could be involved in the failure of cell mediated immunity that is responsible for severe immune-depression in VL.
year | journal | country | edition | language |
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2004-10-01 | Immunology |