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RESEARCH PRODUCT
Impaired cellular immune responses in chronic renal failure: Evidence for a T cell defect
Peter KurzKarl Hermann Meyer Zum BüschenfeldeHans KöhlerStephan MeuerT. H. Hütterothsubject
AdultMaleIsoantigensT-LymphocytesLymphocyteT cellLymphocyte CooperationRenal functionStimulationchemical and pharmacologic phenomenaLymphocyte ActivationLeukocyte CountImmune systemmedicineHumansLymphocytesImmunodeficiencyAgedUremiaB-LymphocytesImmunity Cellularbiologybusiness.industryAntibodies MonoclonalMiddle Agedmedicine.diseaseIn vitromedicine.anatomical_structureNephrologyConcanavalin AAntibody FormationImmunologybiology.proteinInterleukin-2Kidney Failure ChronicFemaleMitogensbusinessdescription
Impaired cellular immune responses in chronic renal failure: Evidence for a T cell defect. Cellular immune responses in vitro were studied in 24 patients on chronic hemodialysis and 16 healthy volunteers with normal kidney function. Patients on maintenance hemodialysis had lymphopenia with diminished numbers of both T4 + and T8 + T-lymphocytes. The T4/T8 ratios were within the normal range. Peripheral blood lymphocytes (PBL) showed a diminished proliferative response upon stimulation with concanavalin A, phytohemagglutinin and poke weed mitogen. When cell surface antigens were used for stimulation (mixed lymphocyte culture) uremic lymphocytes also showed a lower proliferation rate. Although without statistical conformation, there was a tendency by uremic PBL to produce less IL-2 as compared to healthy controls. Moreover, in a PWM driven system, peripheral blood lymphocytes from uremics produced significantly less IgG than PBL from normals. These results support the notion that a profound defect in lymphocyte function accounts at least, in part, for the observed immunodeficiency of uremic patients.
year | journal | country | edition | language |
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1986-06-01 | Kidney International |