Interleukin-10 and acute rejection in renal transplantation

Interleukin-10-1082 G/a polymorphism and acute renal graft rejection: a meta-analysis

“…41 For example, Hutchings et al 27 performed a study to determine the distribution of IL-10-1082 (G/A) promoter polymorphism in African-American and Caucasian renal transplant recipients, then he found that there was a significant link between IL-10 genotype and AREs, but only in African-American patients (p50.01). Among our included studies, six studies 11,16,18,24,26,31 were in research of Caucasian recipients, two studies 27,32 were in research of both Caucasian and African-American recipients, and the others did not refer to ethnicity. Nevertheless, when stratifying for ethnicity, no significant association was observed.…”

“…It is necessary to mention the relatively limited power of our meta-analysis to find a different result. For example, the country zones of the 22 studies were unevenly distributed, in which, 10 researches 11,16,18,20,21,25,[28][29][30]32 were from Europe, six researches 12,14,15,17,19,22 were from Asia, 5 researches 23,24,26,27,31 were from America, and only one research 13 was from Africa. Another drawback that might influence our study results is the insufficient information among the included studies, encompassing ethnicity, age, gender, HWE deviations, etc.…”

‐174G/C interleukin‐6 gene polymorphism and the risk of transplanted kidney failure or graft loss during a 5‐year follow‐up period

“…Under the kidney transplantation setting, a variety of cytokine and chemokine gene polymorphisms have been investigated in terms of favourable or detrimental graft survival. These include, for example, IL‐1α, IL‐1β, IL‐2, IL‐4, IL‐6, IL‐10, TGF‐β, TNF‐α, TNF‐β, INF‐γ, chemokine (C‐C motif) receptor (CCR)2, CCR5 and monocyte chemoattractant protein‐1 (2–4, 7, 8, 10–17). Among those mentioned above, IL‐10 and TNF‐α cytokine genes have been previously reported as relevant to allograft outcome (7, 8, 11, 18–20), although some authors did not confirm these results (4, 6, 21) or obtained ambiguous findings (22).…”

“…These include, for example, IL‐1α, IL‐1β, IL‐2, IL‐4, IL‐6, IL‐10, TGF‐β, TNF‐α, TNF‐β, INF‐γ, chemokine (C‐C motif) receptor (CCR)2, CCR5 and monocyte chemoattractant protein‐1 (2–4, 7, 8, 10–17). Among those mentioned above, IL‐10 and TNF‐α cytokine genes have been previously reported as relevant to allograft outcome (7, 8, 11, 18–20), although some authors did not confirm these results (4, 6, 21) or obtained ambiguous findings (22). In addition, IL‐6, TGF‐β and INF‐γ genotypes have also been found to have an influence on the incidence of AR episodes or DGF (7, 8, 10, 13).…”

Systemic Overexpression of Interleukin-10 Fails to Protect Allogeneic Islet Transplants in Nonobese Diabetic Mice

“…IL-10 is also considered a major contributor to the mechanisms underlying immune tolerance to alloantigens by inducing alloreactive CD4 ϩ T cells to acquire regulatory cell functions (6). Furthermore, a body of literature has documented the efficacy of IL-10 in protection of allogeneic transplants from acute and chronic rejection in solid organ transplantations including lung, kidney, heart, and liver (7)(8)(9)(10). Although IL-10 treatment has not been extensively investigated in allogeneic islet transplantation, several lines of evidence would suggest its potential efficacy, including in vitro inhibition of allogeneic lymphocyte proliferation (11) and in vivo prevention of primary islet nonfunction by IL-10 (12).…”