Aberrant Recruitment and Activation of T Cells in Diabetic Nephropathy

Moon, Jae‐Young; Jeong, Kyung-Hwan; Lee, Tae-Won; Ihm, Chun-Gyoo; Lim, Sung Jig; Lee, Sang-Ho

doi:10.1159/000334928

Cited by 140 publications

(126 citation statements)

References 60 publications

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“…This indicates that IL-7 can contribute to the pathogenesis of autoimmune diabetes by enabling effector/memory T cells to remain in a functionally competent state. In a recent study, an aberrant recruitment and activation of effector T cells in T2D-associated nephropathy was demonstrated, and found to be correlated with the amount of proteinuria [42]. As such, the increased IL-5 and IL-7 levels detected in the prediabetic African American females in our study might indicate that they are at increased risk to develop diabetic nephropathy.…”

Section: Discussionsupporting

confidence: 58%

Cytokine profiling of young overweight and obese female African American adults with prediabetes

et al. 2013

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Approximately 5–10% of subjects with prediabetes become diabetic every year. Inflammation is involved in the development of obesity-related type 2 diabetes (T2D). However, to date, the relationship between inflammation and prediabetes, defined by hemoglobin A1c (HbA1c) ≥ 5.7 and < 6.5%, remains largely unexplored, especially in African Americans. Therefore, in this study we examined a comprehensive panel of 13 cytokines involved in the inflammatory response in overweight/obese subjects with prediabetes. A total of 21 otherwise healthy, overweight/obese, young adult African American females with prediabetes, together with 20 matched overweight/obese controls, were selected for this study. Plasma cytokines were assessed by multiplex cytokine profiling. Plasma concentrations of interleukin (IL)-5, IL-6, IL-7, tumor necrosis factor-α (TNF-α), and granulocyte-monocyte colony-stimulating factor (GM-CSF) were significantly higher in the prediabetic group, as compared to the control group (all p < 0.05). Plasma concentrations of all the other cytokines, interferon-γ (IFN-γ), IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70 and IL-13, seemed to be elevated in the prediabetic group, but failed to reach statistical significances. Upon merging both groups, HbA1c was found to be positively correlated with IFN- γ, IL-1β, IL-2, IL-5, IL-7, IL-8, TNF-α and GM-CSF. This study demonstrates elevated levels of various pro-inflammatory cytokines in overweight/obese young subjects with prediabetes, which place them at higher risk of developing T2D and cardiovascular diseases. Our data also call for further investigations in animal models and population cohorts to establish the roles of a variety of pro-inflammatory cytokines in the early development of obesity-related T2D.

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Section: Discussionsupporting

confidence: 58%

Cytokine profiling of young overweight and obese female African American adults with prediabetes

et al. 2013

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“…The first contribution of the studies was about the increase in local accumulating T cells in diabetic experimental models. Xiao et al [10] and Moon et al [11] showed an increase in CD4 and CD8 lymphocytes in diabetic mouse, these changes were observed in glomeruli and interstice.…”

Section: T Lymphocytesmentioning

confidence: 92%

Diabetic nephropathy and inflammation

Durán-Salgado¹

2014

WJD

343

234

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Diabetic nephropathy (DN) is the leading cause of end-stage renal failure worldwide. Besides, diabetic nephropathy is associated with cardiovascular disease, and increases mortality of diabetic patients. Several factors are involved in the pathophysiology of DN, including metabolic and hemodynamic alterations, oxidative stress, and activation of the renin-angiotensin system. In recent years, new pathways involved in the development and progression of diabetic kidney disease have been elucidated; accumulated data have emphasized the critical role of inflammation in the pathogenesis of diabetic nephropathy. Expression of cell adhesion molecules, growth factors, chemokines and pro-inflammatory cytokines are increased in the renal tissues of diabetic patients, and serum and urinary levels of cytokines and cell adhesion molecules, correlated with albuminuria. In this paper we review the role of inflammation in the development of diabetic nephropathy, discussing some of the major inflammatory cytokines involved in the pathogenesis of diabetic nephropathy, including the role of adipokines, and take part in other mediators of inflammation, as adhesion molecules.

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“…Bending and colleagues observed in the renal parenchyma that the absolute number and percent of activated T-lymphocytes in the renal parenchyma was significantly higher in insulin dependent patients with diabetes with proteinuria than without proteinuria [16,31]. CD3+ T cells have also been found in the interstitium of mice with streptozotocin induced diabetes and proteinuria [32].T cells infiltrating the diabetic kidney produce inflammatory cytokines, such as TNF-α, interleukin-6 and interferon-γ. These T cells likely contribute to local inflammation and tissue damage [32,33].…”

Section: Role Of T Lymphocytes In Diabetic Nephropathymentioning

confidence: 99%

“…CD3+ T cells have also been found in the interstitium of mice with streptozotocin induced diabetes and proteinuria [32].T cells infiltrating the diabetic kidney produce inflammatory cytokines, such as TNF-α, interleukin-6 and interferon-γ. These T cells likely contribute to local inflammation and tissue damage [32,33]. Using db/db mice Eller et al have recently shown that suppressing the activity of T cells prevents development of diabetic nephropathy.…”

Section: Role Of T Lymphocytes In Diabetic Nephropathymentioning

confidence: 99%

“…B cells appear to infiltrate the kidney of patients with type 2 diabetes, but it remains unclear if these cells directly cause tissue injury [32]. Evidence of glomerular immune complex deposition and increased autoantibodies titers in sera of diabetic patients and mouse models of diabetic nephropathy implicate B cells in the mechanism of diabetic nephropathy.…”

Section: Proposed Role Of B Lymphocytes and Autoantibodies In Diabetimentioning

confidence: 99%

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The Role of the Immune System in the Pathogenesis of Diabetic Nephropathy

Velez¹,

Bhalla²

2012

10.4172/2161-0959.10001J Nephrol Therapeutic30

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Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD) in adults. Despite our current understanding of the disease, we cannot accurately predict which patients with diabetes will develop nephropathy, and we cannot halt the progression to ESRD. Research on the role of the immune system in DN may shed light on novel biomarkers and therapies for this severe complication of diabetes mellitus. In this review we examine the current knowledge of the role of immune system in the development and progression of diabetic nephropathy, speculate on the potential role of B lymphocytes, and highlight implications for prognosis and therapy.

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Aberrant Recruitment and Activation of T Cells in Diabetic Nephropathy

Cited by 140 publications

References 60 publications

Cytokine profiling of young overweight and obese female African American adults with prediabetes

Cytokine profiling of young overweight and obese female African American adults with prediabetes

Diabetic nephropathy and inflammation

The Role of the Immune System in the Pathogenesis of Diabetic Nephropathy

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