Browsing by Author "Milovancevic, Mina (57236937100)"

Background: Previous studies suggested an important role of impairments in T cell subsets in different stages during type 1 diabetes (T1D) development, while data regarding CD25high T cells and transforming growth factor β1 (TGFβ1), both T regulatory associated, remains controversial. We analyzed the level of (a) CD25high T cells (b) TGFβ1 in 17 first-degree relatives of patients with T1D in stage 1 (FDRs1) (GADA+, IA-2+); 34 FDRs in stage 0 (FDRs0) (GADA-, IA-2-); 24 recent-onset T1D in insulin-requiring state (IRS); 10 patients in clinical remission (CR); 18 healthy, unrelated controls (CTR). Methods: T cell subsets were characterized by two-color immunofluorescence staining and flow cytometry; TGFβ1 was determined by ELISA, GADA, and IA-2 by RIA. Results: The percentage of CD25high T cells in FDRs1 was lower than controls, FDRs0, IRS, and CR (p<0.001). Additionally, the cut-off value for CD25high = 1.19%, with a probability of 0.667, for having a higher risk for T1D. TGFβ1 concentration in FDRs1, FDRs0, IRS, and CR, was lower than controls (p<0.001). IRS has a higher TGFβ1 concentration than CR (p<0.001). Conclusions: Stage 1, a higher risk for T1D, is characterized by decreases in CD25high T cells and TGFβ1, partially reflecting impaired T regulatory response, implying that changes of this T cells subset might be a risk marker for T1D. FDRs, irrespective of risk for T1D and T1D patients irrespective of state, had depletion of TGFβ1, suggesting the association of TGFβ1 could have potential with familiar risk and manifestation of T1D. Furthermore, the result suggested that the clinical course of overt T1D might be modulated on the TGFβ1 level. © 2024 Society of Medical Biochemists of Serbia. All rights reserved.

Background: Previous studies suggested an important role of impairments in T cell subsets in different stages during type 1 diabetes (T1D) development, while data regarding CD25high T cells and transforming growth factor β1 (TGFβ1), both T regulatory associated, remains controversial. We analyzed the level of (a) CD25high T cells (b) TGFβ1 in 17 first-degree relatives of patients with T1D in stage 1 (FDRs1) (GADA+, IA-2+); 34 FDRs in stage 0 (FDRs0) (GADA-, IA-2-); 24 recent-onset T1D in insulin-requiring state (IRS); 10 patients in clinical remission (CR); 18 healthy, unrelated controls (CTR). Methods: T cell subsets were characterized by two-color immunofluorescence staining and flow cytometry; TGFβ1 was determined by ELISA, GADA, and IA-2 by RIA. Results: The percentage of CD25high T cells in FDRs1 was lower than controls, FDRs0, IRS, and CR (p<0.001). Additionally, the cut-off value for CD25high = 1.19%, with a probability of 0.667, for having a higher risk for T1D. TGFβ1 concentration in FDRs1, FDRs0, IRS, and CR, was lower than controls (p<0.001). IRS has a higher TGFβ1 concentration than CR (p<0.001). Conclusions: Stage 1, a higher risk for T1D, is characterized by decreases in CD25high T cells and TGFβ1, partially reflecting impaired T regulatory response, implying that changes of this T cells subset might be a risk marker for T1D. FDRs, irrespective of risk for T1D and T1D patients irrespective of state, had depletion of TGFβ1, suggesting the association of TGFβ1 could have potential with familiar risk and manifestation of T1D. Furthermore, the result suggested that the clinical course of overt T1D might be modulated on the TGFβ1 level. © 2024 Society of Medical Biochemists of Serbia. All rights reserved.

Background/Objectives: Previous studies reported impairments in insulin secretion during different stages of type 1 diabetes (T1D), while data regarding insulin sensitivity and immunological changes are still controversial. We analyzed the following: (a) insulin secretion, (b) insulin sensitivity, and (c) pro-inflammatory interleukin-17 (IL-17) levels in peripheral blood in 17 healthy first-degree relatives in stage 1 (FDRs1) (GAD+, IA2+), 34 FDRs in stage 0 (FDRs0) (GAD−, IA2A−), 24 recent-onset T1D (R-T1D) patients in the insulin-requiring state (IRS), 10 in clinical remission (CR), and 18 healthy unrelated controls (HC). Methods: Insulin secretion was evaluated by an IVGTT and a glucagon stimulation test, expressed as a first-phase insulin response (FPIR) and a basal/stimulated C-peptide. Insulin sensitivity was tested by the euglycemic hyperinsulinemic clamp, expressed as an M value. Results: FDRs1 had a lower FPIR than FDRs0 (p < 0.05) and HC (p < 0.001) but higher than RT1D-IRS (p < 0.001) and RT1D-CR (p < 0.01). Moreover, FDRs1 had lower basal/stimulated C-peptide than FDRs0 (p < 0.01/p < 0.05) and HC (p < 0.001/p = 0.001) but higher levels than RT1D-IRS (p < 0.001/p < 0.001). However, the M value was similar among FDRs1, FDRs0, and HC (p = 1.0) but higher than RT1D-IRS (p < 0.001) and RT1D-CR (p < 0.01), while RT1D-IRS and RT1D-CR had lower M than HC (p < 0.001; p < 0.001; respectively). FDRs1 had higher IL-17 than FDRs0 (p < 0.001) and HC (p < 0.05). RT1D-IRS had higher IL-17 than FDRs0 (p < 0.001) and HC (p < 0.001), which was similar to RT1D-CR vs. FDRs0 (p < 0.001) and HC (p < 0.05). Conclusions: Early changes in pre-T1D might involve an initial decline of insulin secretion associated with a pro-inflammatory attack, which does not influence insulin sensitivity, whereas later, insulin sensitivity deterioration seems to be associated with the prominent reduction in insulin secretion. © 2025 by the authors.