Putative loss of CD83 immunosuppressive activity in long-standing complication-free juvenile diabetic patients during disease progression.

The CD83 molecule is a known marker of dendritic cell differentiation process, and its soluble form (sCD83) exerts immunosuppressive functions. In our research, we examined whether the sCD83 plasma concentration is impaired in DM1 children and if the expected changes are in line with the disturbed process of monocyte's transformation into mCD83 monocyte-derived cells. 28 newly diagnosed (ND-DM1) and 30 long-standing (LS-DM1) patients were enrolled into our study.

Monocytes of newly diagnosed juvenile DM1 patients are prone to differentiate into regulatory IL-10 M2 macrophages.

Alternatively activated macrophages (M2) exert anti-inflammatory effects and are crucial for keeping balance between protective and destructive cell-mediated immunity in healing phase of inflammation. Two members of the interferon regulatory factors family, IRF5 and IRF4, are known to promote M1 or M2 phenotype, respectively. Our study aimed to analyse the effectiveness of the M2 differentiation process in vitro (achieved by IL-4 stimulation) and its relationship to the stage of type 1 diabetes mellitus (DM1) in juvenile patients.

CD34+ and CD34+VEGFR2+ cells in poorly controlled hypertensive patients.

CD34+ and CD34+VEGFR2+ cells participate in the repair of damaged endothelium and vascular remodelling. As their number and activity change due to the development of cardiovascular diseases, they are recognised as useful markers of cardiovascular health. As ineffective blood pressure control concerns high percentage of hypertensive patients, the purpose of our study was to investigate if proportions of various CD34+ and CD34+VEGFR2+ populations change due to hypertension occurrence and the effectiveness of the therapy.

CCR5-Δ32 polymorphism is a genetic risk factor associated with dyslipidemia in patients with type 1 diabetes.

Aim: In the currently available literature there are no works investigating the correlation between CCR5-Δ32 polymorphism and dyslipidemia in children with type 1 diabetes mellitus (T1D). Therefore, we have decided to explore the potential role played by this polymorphic locus in the incidence of dyslipidemia as an important risk factor for cardiovascular disease (CVD) in patients with T1D.

Methods: A total of 380 patients with T1D were selected.

The KL-VS polymorphism of KLOTHO gene is protective against retinopathy incidence in patients with type 1 diabetes.

Background And Aims: KLOTHO is an anti-ageing circulating hormone involved in insulin signaling, inflammation and vascular homeostasis through its protective effects on the endothelium and antioxidant actions. The common functional "KL-VS" variant of the KLOTHO gene is reproducibly associated with longevity in humans. Large number of studies have evaluated close relationship between KLOTHO protein and diabetes but the association between KL-VS variant and retinopathy in type 1 diabetes mellitus (T1D) is unknown.

Association of circulating progenitor cells with angiotensin II in newly diagnosed hypertensive patients.

Populations of CD34- and VEGFR2-expressing cells are responsible for regeneration of damaged endothelium and vascular remodelling. As their quantity and activity changes during cardiovascular diseases, they are potentially useful markers of cardiovascular health. The aim of our study was to investigate changes of various CD34+ and CD34+ VEGFR2+ populations in subjects with newly recognised hypertension and to evaluate whether observed alterations are influenced by clinical parameters and angiotensin II.

Estrogen receptor α gene polymorphism and vascular complications in girls with type 1 diabetes mellitus.

The effect of estrogens is mediated by activation of estrogen receptors (ERs). Because ER-α gene polymorphisms may exert different effects in childhood, we analyzed the associations between the IVS1 -397T>C (PvuII) polymorphism and systemic inflammatory state, proangiogenic factors, frequency of monocyte subsets, lipid profile, blood pressure, and vascular complications in girls with type 1 diabetes mellitus (DM1). We examined 180 young girls with DM1 and 120 healthy age-matched controls.

ScaI atrial natriuretic peptide gene polymorphisms and their possible association with postoperative atrial fibrillation - a preliminary report.

Introduction: Atrial fibrillation (AF) is a frequently encountered complication after coronary artery bypass grafting (CABG), but its underlying mechanisms are still unclear. The natriuretic peptides have been reported as markers for predicting the occurrence of postoperative AF. This study evaluates whether the ScaI ANP gene polymorphisms predict the occurrence of postoperative AF.

CCR5-Δ32 gene polymorphism is related to celiac disease and autoimmune thyroiditis coincidence in patients with type 1 diabetes.

Aim: The aim of the study was to assess the relationship between CCR5-Δ32 polymorphism and the coincidence of celiac and autoimmune thyroid diseases with type 1 diabetes mellitus (T1D) in children.

Methods: 420 children with T1D aged 15.5±3.

IL-33 Effect on Quantitative Changes of CD4CD25FOXP3 Regulatory T Cells in Children with Type 1 Diabetes.

IL-33 is an IL-1 cytokine family member, with ability to induce both Th1 and Th2 immune responses. It binds to ST2 receptor, whose deficiency is associated with enhanced inflammatory response. The most recent studies have shown the immunoregulatory effect of IL-33 on Tregs in animal models.

CCR5-Δ32 gene polymorphism is associated with retinopathy in patients with type 1 diabetes.

Aim: The aim of the study was to assess the relationship between the CCR5-Δ32 polymorphism and the risk of diabetic retinopathy (DR) in patients with DM1.

Methods: We examined 420 patients and 350 healthy controls. The analysis concerned CCR5-Δ32 polymorphism as well as levels of serum inflammatory markers (CRP, TNF-α), adhesion molecules (VCAM, ICAM-1, ICAM-3) and CCR5 ligand (MCP-1).

The GG genotype of the -152 G/A vascular endothelial growth factor (VEGF) polymorphism predisposes to hypertension-related chronic kidney disease.

Our purpose was to determine whether the VEGF -152 G/A polymorphism could be associated with chronic kidney disease and endothelial dysfunction in hypertensive patients. There were 100 healthy volunteers enrolled into the control group. The group of patients was constituted by 99 consecutively admitted hypertensive patients referred to our Institution by their general practitioner.

Vascular endothelial growth factor polymorphism (-460 T/C) is related to hypertension-associated chronic kidney disease.

Our aim was to characterize the endothelial progenitor cells (EPCs) in normotensive controls and treated hypertensive individuals within the vascular endothelial growth factor (VEGF) -460 C/T polymorphism as well as to investigate whether this polymorphism predisposes to hypertension-related chronic kidney disease. The hypertensive patients bearing the TT genotype had the highest levels of immature EPC with the following phenotypes: CD34(+), CD34(+)CD45(dim), CD34(+)CD133(+)CD45(dim). The study showed the estimated glomerular filtration rate values significantly lower and creatinine and BUN parameters higher among the TT hypertensive patients.

The GA genotype of the -1154 G/A (rs1570360) vascular endothelial growth factor (VEGF) is protective against hypertension-related chronic kidney disease incidence.

Vascular endothelial growth factor (VEGF) is a highly specific mitogen with angiogenic and vascular permeability activities for endothelial cells. VEGF participates in maintaining the renal vasculature integrity. There is no doubt that hypertension accelerates progression to renal dysfunction, resulting in chronic kidney disease (CKD).

Th9 and Th22 immune response in young patients with type 1 diabetes.

Th17, Th22 and Th9 are recently discovered effector populations that may contribute to the pathogenesis of autoimmune and inflammatory diseases. The presented study aimed to investigate the link between Th22 and Th9 subsets in type 1 diabetes, as this disease involves different subsets of CD4+ T lymphocytes. The study groups consisted of 23 patients with type 1 diabetes and 11 healthy individuals.

Elevated levels of peripheral blood CD14(bright) CD16+ and CD14(dim) CD16+ monocytes may contribute to the development of retinopathy in patients with juvenile onset type 1 diabetes.

The study aimed to analyze the CD14(bright) CD16(+) and CD14(dim) CD16(+) monocyte subsets in juvenile-onset complication-free diabetes mellitus type 1 in the context of their association with microvascular complications. 61 children with type 1 diabetes and 30 healthy individuals were enrolled in a study. CD14(bright) CD16(+) and CD14(dim) CD16(+) monocytes were quantified in peripheral blood by means of flow cytometry.

Grade of inflammation in boys with type 1 diabetes depends on the IVS1 -397T>C estrogen receptor α polymorphism.

Background And Aims: The effect of estrogens is mediated by activation of estrogen receptors (ERs), which are expressed in many tissues. Because ER-α gene polymorphisms may exert different effects in childhood, in the present study we analyzed associations between the IVS1 -397T>C polymorphism and indicators of inflammatory response as well as late complications in boys with type 1 diabetes mellitus (DM1).

Methods And Results: We examined 108 young boys with DM1 and 64 healthy age-matched control individuals.

Different pathways of macrophage activation and polarization.

Monocytes are short-lived cells and undergo spontaneous apoptosis every day. Inflammatory responses may induce dramatic up-regulation of monocyte survival and differentiation. When monocytes are recruited to an area of infection they may differentiate into macrophages.

Cytokine profiles during delivery affect cord blood hematopoietic stem and progenitors cells.

The study was aimed to determine the correlations between serum levels of cytokines (GM-CSF, IL-4, IL-10 and TNF) in maternal (MB) and cord blood (CB) and some features of cord blood hematopoietic stem and progenitor cells (CB HSPCs). Study material was MB and concomitant CB samples collected from 98 volunteers at the moment of delivery. The IL-4, IL-10, TNF and GM-CSF concentrations in serum and in supernatants from PMA-stimulated mononuclear cells isolated from both blood types were measured using BD Cytometric Bead Array Flex Set System.

Enhanced apoptosis of monocytes from complication-free juvenile-onset diabetes mellitus type 1 may be ameliorated by TNF-α inhibitors.

Diabetes mellitus type 1 is associated with an enhanced apoptosis of different cells and tissues, accelerating occurrence of diabetic microvascular complications. The aim of our study was to determine spontaneous apoptotic potential of the monocyte subsets in juvenile-onset complication-free diabetes mellitus type 1 and to compare them with the corresponding values of the healthy. Moreover, we wanted to assess effects of TNF-R1 blocking agents and those of general TNF-α blocker (Infliximab) on spontaneous apoptosis of monocytes.

Elevated levels of serum IL-12 and IL-18 are associated with lower frequencies of CD4(+)CD25 (high)FOXP3 (+) regulatory t cells in young patients with type 1 diabetes.

Type 1 diabetes is thought to involve chronic inflammation, which is manifested by the activation and expression of different inflammatory mediators. IL-12 and IL-18 are two cytokines that have been shown to exert strong proinflammatory activity and have been implicated in the pathogenesis of type 1 diabetes in mice and humans. The overproduction of proinflammatory mediators is controlled by specialized T cell subset, namely regulatory T cells that express FOXP3 transcription factor.

Effector and regulatory T cell subsets in diabetes-associated inflammation. Is there a connection with ST2/IL-33 axis? Perspective.

Type 1 diabetes (DM1) is a chronic inflammatory disease, which when progresses leads to the development of late vascular complications. The disease involves impairments in regulatory and effector subsets of T lymphocytes, which suppress and maintain inflammatory response, respectively. ST2/IL-33 pathway is involved in T-cell-mediated immune response and might regulate the inflammatory process in several diseases.

IVS1 -397T>C estrogen receptor α polymorphism is associated with low-grade systemic inflammatory response in type 1 diabetic girls.

Purpose: The study aimed to investigate the influence of estrogen receptor α (ER-α) genotypes on inflammatory response and development of microvascular complications in girls with type 1 diabetes.

Methods: 152 young regularly menstruating girls with diagnosed type 1 diabetes and 84 young, healthy menstruating girls were recruited. ER-α genotyping was carried out by PCR.

Treatment of graft-versus-host disease with naturally occurring T regulatory cells.

A significant body of evidence suggests that treatment with naturally occurring CD4(+)CD25(+) T regulatory cells (Tregs) is an appropriate therapy for graft-versus-host disease (GvHD). GvHD is a major complication of bone marrow transplantation in which the transplanted immune system recognizes recipient tissues as a non-self and destroys them. In many cases, this condition significantly deteriorates the quality of life of the affected patients.

The serum IL-6 profile and Treg/Th17 peripheral cell populations in patients with type 1 diabetes.

IL-6 is a pleiotropic cytokine involved in the regulation of the immune response, inflammation, and hematopoeisis. Its elevated levels are found in a range of autoimmune and chronic inflammatory diseases. IL-6 is also involved in regulation of the balance between two T cell subsets: Tregs and Th17, which have contradictory functions in the control of inflammation.