Mixed Lymphocyte Reaction-Induced Release of Soluble Il-2 Receptor

Degiannis, Dimitrios; Czarnecki, Margaret; Hornung, Nete; Rašková, Jana; Raska, K

doi:10.1097/00007890-199102000-00047

Cited by 14 publications

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“…36 The release of sIL-2R is an IL-2 dependent phenomenon. 37 We conclude that the demonstration of increased serum slL-2R levels in patients with UC suggests an enhanced T-cell activation in this disorder. However, the overlaps between different disease stages, and between patients and controls, limit the general diagnostic value of this measure.…”

Section: Discussionmentioning

confidence: 66%

Soluble interleukin‐2 receptors in ulcerative colitis

Nielsen

Brynskov

1993

Mediators of Inflammation

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T-Cell activation results in the release or shedding of a soluble form (45 kDa) of the cellular (55 kDa) low-affinity interleukin-2 receptor (α-chain) (slL-2R). The present study was performed to investigate if the serum concentration of sIL-2R is a marker of disease activity in patients with ulcerative colitis (UC), a chronic inflammatory bowel disease. Twenty-seven UC patients (about half of them in remission) and 13 healthy volunteers were studied, sIL-2R concentrations were measured by an enzyme-linked immunosorbent assay, and significantly elevated median sIL-2R values were found in clinically active UC (150 pg/ml; range 100–420), compared to inactive UC (145 pg/ml; range 110–255), and healthy controls (110 pg/ml; range 80–165) (p < 0.01). There was no correlation between sIL-2R concentrations and extent of the disease. Due to the overlap of serum sIL-2R concentrations between different disease stages and controls, the general diagnostic value seems to be limited. However, since slL-2R release is an IL-2 dependent phenomenon, we conclude that the demonstration of increased serum sIL-2R concentrations in UC suggests the existence of an enhanced T-cell activation in vivo in this disease. Further longitudinal studies are required to elucidate if repeated measurements of sIL-2R levels provide an additional way of monitoring UC disease activity in individual patients.

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Section: Discussionmentioning

confidence: 66%

Soluble interleukin‐2 receptors in ulcerative colitis

Nielsen

Brynskov

1993

Mediators of Inflammation

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“…It has previously been shown that MSCs decrease membrane-bound IL-2Ra on PBLs stimulated by PHA [11]. IL-2Ra also exists in a soluble form (sIL-2R), which is secreted by activated T cells [17,18]. The release of IL-2R is inhibited by immunosuppressive drugs such as rapamycin and cyclosporin A (CsA) [19].…”

Section: Human Mesenchymal Stem Cells (Mscs) Inhibit T-cell Responsesmentioning

confidence: 99%

Mesenchymal stem cells inhibit lymphocyte proliferation by mitogens and alloantigens by different mechanisms

Rasmusson

Ringdén

Sundberg

et al. 2005

Experimental Cell Research

452

316

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“…Even if exogenous rhIL-2 was present in the MLR, the inhibitory effect of ACs overcame the acceleration of the MLR. Thus, human ACs induce IL-2 nonresponsiveness in allogeneic lymphocytes sIL-2R is secreted by activated CD4 + T cells, 11,12 and the sIL-2R concentration has been proposed as a marker of rejection episodes after organ transplantation. 13,14 Acute renal allograft rejection is mediated by T lymphocytes; T cells expressing cell surface IL-2R were present in the kidneys of renal allograft recipients.…”

Section: Discussionmentioning

confidence: 99%

“…sIL-2R is secreted by activated CD4 + T cells, 11,12 and the sIL-2R concentration has been proposed as a marker of rejection episodes after organ transplantation. 13,14 Acute renal allograft rejection is mediated by T lymphocytes; T cells expressing cell surface IL-2R were present in the kidneys of renal allograft recipients.…”

Section: Discussionmentioning

confidence: 99%

Human Articular Chondrocytes Induce Interleukin-2 Nonresponsiveness to Allogeneic Lymphocytes

2016

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Introduction. We previously showed that articular chondrocytes (ACs) have immune privilege and immunomodulatory functions like those of mesenchymal stem cells. To elucidate these mechanisms, we focused on interleukin-2 (IL-2), which plays critical roles in lymphocyte mitogenic activity. The purpose of this study was to explore whether ACs affect the role of IL-2 underlying immunomodulatory functions. Material and Methods. Irradiated human ACs from osteoarthritis donors were used. Third-party ACs were added to the mixed lymphocyte reaction (MLR) with or without recombinant human IL-2 (rhIL-2), and the levels of IL-2 and the soluble form of the IL-2 receptor α (sIL-2Rα) protein in supernatant were measured by enzyme-linked immunosorbent assay. Recombinant human IL-2 (rhIL-2) was also added to the MLR. To detect the expression of IL-2 receptor α (CD25) on lymphocytes in the MLR, flow cytometric analysis was performed. Last, ACs and allogeneic activated CD4 + T cell were co-cultured, and the expression of CD25 on activated T cells was examined by flow cytometry. Results. Third-party ACs significantly inhibited the MLR and reduced the level of sIL-2Rα in a dose-dependent manner, but did not affect the concentration of IL-2. Exogenous rhIL-2 accelerated MLR but did not rescue the inhibitory effect of ACs. ACs inhibited the expression of CD25 on activated CD4 + T cells. Discussion. Our results showed that thirdparty ACs inhibited the proliferation of allogeneic activated lymphocytes, thereby inhibiting production sIL-2Rα, although ACs did not affect IL-2 secretion from lymphocytes. Also, ACs inhibited CD25 expression on activated CD4 + T cells. Thus, ACs inhibited the immune response of allogeneic lymphocytes by inducing IL-2 nonresponsiveness.

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Mixed Lymphocyte Reaction-Induced Release of Soluble Il-2 Receptor

Cited by 14 publications

References 0 publications

Soluble interleukin‐2 receptors in ulcerative colitis

Soluble interleukin‐2 receptors in ulcerative colitis

Mesenchymal stem cells inhibit lymphocyte proliferation by mitogens and alloantigens by different mechanisms

Human Articular Chondrocytes Induce Interleukin-2 Nonresponsiveness to Allogeneic Lymphocytes

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