title: Immune deficiency in uremia: interleukin-2 production and responsiveness and interleukin-2 receptor expression and release.
abstract: We have studied the role of interleukin-2 (IL-2) and its receptors in the impaired in vitro lymphocyte response characteristic of hemodialysis patients treated by means of cuprophane membranes. The proliferative response of T lymphocytes as well as T-cell-dependent B cell proliferation after stimulation with mitogens was significantly reduced in hemodialysis patients. The in vitro production of IL-2 after such stimulation in parallel cultures was found to be similar in patients and in controls. The expression of IL-2 receptor on the lymphocyte cellular membrane in the hemodialysis group was also similar to controls. The in vitro proliferative response of uremic lymphocytes to exogenous IL-2, however, was significantly depressed suggesting a reduced availability of biologically active IL-2 receptor. The release of soluble IL-2 receptor by lectin-stimulated lymphocytes in culture was also significantly lower in the patient group; yet, hemodialysis patients has a strikingly elevated level of plasma soluble IL-2 receptor, and similar high levels were also found in three other groups of end-stage renal disease patients dialyzed by means of cellulose acetate, polysulfone and polyacrylonitrile membranes, as well as in a group of uremic patients on conservative treatment. In the hemodialysis patient group a significant positive correlation between levels of soluble IL-2 receptor and the duration of hemodialysis was found. Since soluble IL-2 receptor has been reported to down-regulate lymphocyte responses, the elevation in plasma levels of soluble IL-2 receptor in hemodialysis patients may be a pathogenetic factor in the progressive development of impaired immunity associated with end-stage renal disease.
authors.affiliation: Department of Pathology, UMDNJ-Robert Wood Johnson Medical School, Piscataway.
authors.forename: D
authors.initials: D
authors.lastname: Donati
authors.forename: D
authors.initials: D
authors.lastname: Degiannis
authors.forename: L
authors.initials: L
authors.lastname: Homer
authors.forename: L
authors.initials: L
authors.lastname: Gastaldi
authors.forename: J
authors.initials: J
authors.lastname: Raskova
authors.forename: K
authors.initials: K
authors.lastname: Raska
mesh_terms: D000368:Aged; D002452:Cell Count / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D007153:Immunologic Deficiency Syndromes / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D007376:Interleukin-2 / Q000378:metabolism* / Q000494:pharmacology; D037102:Lectins / Q000494:pharmacology; D008214:Lymphocytes / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D008875:Middle Aged; D008934:Mitogens / Q000494:pharmacology; D010641:Phenotype; D015375:Receptors, Interleukin-2 / Q000097:blood / Q000378:metabolism*; D011994:Recombinant Proteins / Q000494:pharmacology; D006435:Renal Dialysis; D014511:Uremia / Q000150:complications* / Q000378:metabolism / Q000473:pathology
chemical_list: D007376:Interleukin-2; D037102:Lectins; D008934:Mitogens; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins