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Accessory cell functions in mononuclear cell cultures uremic patients
1Medical Department P, Rigshospitalet, Copenhagen, Denmark.
Insights
Dialysis patients exhibit reduced lymphocyte proliferation, particularly in response to T cell stimulation. Interleukin-2 (IL-2) partially restored this response, suggesting uremia primarily affects T cell proliferation.
Area of Science:
- Immunology
- Nephrology
- Cellular Biology
Background:
- Uremia, a condition associated with kidney failure, can lead to immune system dysregulation.
- T cell dysfunction is a recognized complication in patients with chronic kidney disease undergoing dialysis.
Purpose of the Study:
- To investigate T cell responses in dialyzed patients.
- To determine the effects of Interleukin-1 (IL-1) and Interleukin-2 (IL-2) on T cell proliferation in uremia.
- To assess the role of accessory cells in uremic T cell dysfunction.
Main Methods:
- Isolation of peripheral blood mononuclear cells (PBMC) from dialyzed patients and healthy controls.
- Stimulation of lymphocytes with phytohemagglutinin (PHA) and T cell receptor antibody (Leu 4).
- Assessment of T cell proliferation with and without exogenous IL-1 and IL-2, and with normal accessory cells.
Main Results:
- Lymphocyte proliferation responses to PHA and Leu 4 stimulation were decreased in patient cultures.
- IL-2 alone significantly enhanced, and nearly normalized, the proliferation of T cells stimulated with suboptimal PHA concentrations.
- IL-1 did not improve proliferation, and no additive effect was observed with combined IL-1 and IL-2.
- Uremic accessory cells did not impair T cell responses, indicating they support T cell activation.
Conclusions:
- Uremia appears to primarily impair T cell proliferation rather than T cell activation.
- Decreased IL-2 production and the observed effects of exogenous IL-2 suggest a specific role for IL-2 in uremic T cell dysfunction.
- Uremic accessory cells do not suppress T cell responses, challenging previous assumptions about their role.
Abstract:
Mononuclear cells (PBMC) were isolated from dialyzed patients and healthy control subjects. Lymphocyte responses to stimulation with optimal and suboptimal concentrations of lectin (PHA), or stimulation with T cell receptor antibody (Leu 4) were found decreased in the patient cultures. The separate and the combined effects of exogenous interleukin-1 (IL-1) and interleukin-2 (IL-2) were examined in PHA and Leu 4 stimulated cell cultures. Addition of IL-1 did not normalize the decreased proliferation response of the patient cultures. In contrast, addition of IL-2 alone clearly enhanced and almost normalized the response of patient cultures stimulated with suboptimal concentrations of PHA. The combined addition of IL-1 and IL-2 gave no evidence of an additive effect of IL-1 and IL-2. Cell cultures from uremic and normal HLA-identical relative were examined. Substitution of uremic adherent monocytes with normal adherent monocytes as accessory cells did not improve the uremic T cell responses to stimulation with PHA. Furthermore, uremic adherent cells did not suppress the normal T cell responses. These results suggest that uremic accessory cells support T cell activation and, in particular, do not suppress T cell responses. The effect of IL-2 in the present study as well as previous findings of decreased IL-2 production in patients cultures may indicate that uremia primarily influences the proliferation of T cells.
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