Browsing by Author "Stanarcic, Jelena (59663037000)"

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.

We analyzed the level of (a) CXCR3+ (Th1) and CCR4+ (Th2) T memory cells (b) interferon-γ inducible chemokine (IP-10)(Th1) and thymus and activation-regulated chemokine (TARC)(Th2), in 51 first degree relatives (FDRs) of type 1 diabetics (T1D) (17 high risk FDRs (GADA+, IA-2+) and 34 low risk FDRs (GADA-, IA-2-)), 24 recent-onset T1D (R-T1D), and 18 healthy subjects. T memory subsets were analyzed by using four-color immunofluorescence staining and flowcytometry. IP-10 and TARC were determined by ELISA. High risk FDRs showed higher levels of CXCR3+ and lower level of CCR4+ T memory cells compared to low risk FDRs (64.98 ± 5.19 versus 42.13 ± 11.11; 29.46 ± 2.83 versus 41.90 ± 8.58%, resp., P < 0.001). Simultaneously, both IP-10 and TARC levels were increased in high risk versus low risk FDRs (160.12 ± 73.40 versus 105.39 ± 71.30; 438.83 ± 120.62 versus 312.04 ± 151.14 pg/mL, P < 0.05). Binary logistic regression analysis identified the level of CXCR3+ T memory cells as predictors for high risk FDRs, together with high levels of IP-10. The results imply that, in FDRs, the risk for T1D might be strongly influenced by enhanced activity of Th1 and diminished activity of Th2 autoimmune response. © 2014 Tanja Milicic et al.

We analyzed the level of (a) CXCR3+ (Th1) and CCR4+ (Th2) T memory cells (b) interferon-γ inducible chemokine (IP-10)(Th1) and thymus and activation-regulated chemokine (TARC)(Th2), in 51 first degree relatives (FDRs) of type 1 diabetics (T1D) (17 high risk FDRs (GADA+, IA-2+) and 34 low risk FDRs (GADA-, IA-2-)), 24 recent-onset T1D (R-T1D), and 18 healthy subjects. T memory subsets were analyzed by using four-color immunofluorescence staining and flowcytometry. IP-10 and TARC were determined by ELISA. High risk FDRs showed higher levels of CXCR3+ and lower level of CCR4+ T memory cells compared to low risk FDRs (64.98 ± 5.19 versus 42.13 ± 11.11; 29.46 ± 2.83 versus 41.90 ± 8.58%, resp., P < 0.001). Simultaneously, both IP-10 and TARC levels were increased in high risk versus low risk FDRs (160.12 ± 73.40 versus 105.39 ± 71.30; 438.83 ± 120.62 versus 312.04 ± 151.14 pg/mL, P < 0.05). Binary logistic regression analysis identified the level of CXCR3+ T memory cells as predictors for high risk FDRs, together with high levels of IP-10. The results imply that, in FDRs, the risk for T1D might be strongly influenced by enhanced activity of Th1 and diminished activity of Th2 autoimmune response. © 2014 Tanja Milicic et al.