The Experts below are selected from a list of 153 Experts worldwide ranked by ideXlab platform
Martha M Eibl - One of the best experts on this subject based on the ideXlab platform.
-
impaired Primary Immune Response in type 1 diabetes functional impairment at the level of apcs and t cells
Cellular Immunology, 2003Co-Authors: Martin Spatz, Nicole Eibl, Sandra Hink, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Martha M EiblAbstract:We have recently described an impaired proliferative Response of CD4(+) T-cells to Primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. Immunol. 103 (2002) 249]. In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the Immune Response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the Immune Response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the Primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. Taken together, our data suggest that a deviation in the expression of certain molecules known to be involved in the peripheral control of the Immune Response is present in IDDM patients and is underlying the observed impairment of the Primary Immune Response.
-
impaired Primary Immune Response in type 1 diabetes results from a controlled vaccination study
Clinical Immunology, 2002Co-Authors: Nicole Eibl, Martin Spatz, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Aysen Samstag, Martha M EiblAbstract:Patients with diabetes have an increased risk for infections, but information on their adoptive immunity is incomplete and contradictory. Twenty patients with diabetes type-1 and 20 patients with type-2 diabetes were vaccinated with T-cell-dependent Primary protein antigens (hepatitis A viral antigen, HAV; diphtheria toxoid) and a T-cell-independent polysaccharide antigen (pneumococcal polysaccharide). In parallel, the proliferative Response of CD4+ T-cells to the Primary protein antigens keyhole limpet hemocyanin (KLH) and sperm whale myoglobin (SWM) was measured in vitro using monocyte-derived dendritic cells (MDDC) as antigen-presenting cells. Compared to healthy controls, type-1 diabetes patients mounted a significantly impaired Primary antibody Response to hepatitis A vaccine (median HAV antibody titer after the first vaccination, 53 IU/L in diabetic patients vs 212 IU/L in the controls, P = 0.017) and diphtheria toxoid (median serum antibodies after vaccination, patients, 0.94 IU/ml, controls, 6.38 IU/ml, P = 0.004), while the Response to pneumococcal polysaccharide was normal. Type-2 diabetes patients had a comparable metabolic dysregulation but showed a normal antibody Response following vaccination, demonstrating that the effect was not due to hyperglycemia. Antigen-induced interferon-gamma and interleukin-13 release was reduced in type-1 diabetes patients, localizing the impairment to the level of antigen-presenting cell-T-cell interaction. In addition, the proliferative Response of CD4+ T-cells derived from type-1 diabetes patients to KLH and SWM was significantly reduced (P < or = 0.01). FACS analysis of CD80 (B7.1), CD86 (B7.2), and HLA-DR expression on MDDC could not demonstrate significant differences in the expression of these molecules between type-1 and type-2 diabetes patients and healthy controls. An association of low HAV antibody Response with HLA-DR3,4 expression in the patients was shown. Our results indicate that the Primary antibody Response to T-cell dependent antigens as well as the T-cell Response to Primary protein antigens is reduced in type-1 diabetes patients and that additional booster immunization can overcome the defect.
Nicole Eibl - One of the best experts on this subject based on the ideXlab platform.
-
impaired Primary Immune Response in type 1 diabetes functional impairment at the level of apcs and t cells
Cellular Immunology, 2003Co-Authors: Martin Spatz, Nicole Eibl, Sandra Hink, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Martha M EiblAbstract:We have recently described an impaired proliferative Response of CD4(+) T-cells to Primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. Immunol. 103 (2002) 249]. In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the Immune Response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the Immune Response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the Primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. Taken together, our data suggest that a deviation in the expression of certain molecules known to be involved in the peripheral control of the Immune Response is present in IDDM patients and is underlying the observed impairment of the Primary Immune Response.
-
impaired Primary Immune Response in type 1 diabetes results from a controlled vaccination study
Clinical Immunology, 2002Co-Authors: Nicole Eibl, Martin Spatz, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Aysen Samstag, Martha M EiblAbstract:Patients with diabetes have an increased risk for infections, but information on their adoptive immunity is incomplete and contradictory. Twenty patients with diabetes type-1 and 20 patients with type-2 diabetes were vaccinated with T-cell-dependent Primary protein antigens (hepatitis A viral antigen, HAV; diphtheria toxoid) and a T-cell-independent polysaccharide antigen (pneumococcal polysaccharide). In parallel, the proliferative Response of CD4+ T-cells to the Primary protein antigens keyhole limpet hemocyanin (KLH) and sperm whale myoglobin (SWM) was measured in vitro using monocyte-derived dendritic cells (MDDC) as antigen-presenting cells. Compared to healthy controls, type-1 diabetes patients mounted a significantly impaired Primary antibody Response to hepatitis A vaccine (median HAV antibody titer after the first vaccination, 53 IU/L in diabetic patients vs 212 IU/L in the controls, P = 0.017) and diphtheria toxoid (median serum antibodies after vaccination, patients, 0.94 IU/ml, controls, 6.38 IU/ml, P = 0.004), while the Response to pneumococcal polysaccharide was normal. Type-2 diabetes patients had a comparable metabolic dysregulation but showed a normal antibody Response following vaccination, demonstrating that the effect was not due to hyperglycemia. Antigen-induced interferon-gamma and interleukin-13 release was reduced in type-1 diabetes patients, localizing the impairment to the level of antigen-presenting cell-T-cell interaction. In addition, the proliferative Response of CD4+ T-cells derived from type-1 diabetes patients to KLH and SWM was significantly reduced (P < or = 0.01). FACS analysis of CD80 (B7.1), CD86 (B7.2), and HLA-DR expression on MDDC could not demonstrate significant differences in the expression of these molecules between type-1 and type-2 diabetes patients and healthy controls. An association of low HAV antibody Response with HLA-DR3,4 expression in the patients was shown. Our results indicate that the Primary antibody Response to T-cell dependent antigens as well as the T-cell Response to Primary protein antigens is reduced in type-1 diabetes patients and that additional booster immunization can overcome the defect.
Martin Spatz - One of the best experts on this subject based on the ideXlab platform.
-
impaired Primary Immune Response in type 1 diabetes functional impairment at the level of apcs and t cells
Cellular Immunology, 2003Co-Authors: Martin Spatz, Nicole Eibl, Sandra Hink, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Martha M EiblAbstract:We have recently described an impaired proliferative Response of CD4(+) T-cells to Primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. Immunol. 103 (2002) 249]. In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the Immune Response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the Immune Response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the Primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. Taken together, our data suggest that a deviation in the expression of certain molecules known to be involved in the peripheral control of the Immune Response is present in IDDM patients and is underlying the observed impairment of the Primary Immune Response.
-
impaired Primary Immune Response in type 1 diabetes results from a controlled vaccination study
Clinical Immunology, 2002Co-Authors: Nicole Eibl, Martin Spatz, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Aysen Samstag, Martha M EiblAbstract:Patients with diabetes have an increased risk for infections, but information on their adoptive immunity is incomplete and contradictory. Twenty patients with diabetes type-1 and 20 patients with type-2 diabetes were vaccinated with T-cell-dependent Primary protein antigens (hepatitis A viral antigen, HAV; diphtheria toxoid) and a T-cell-independent polysaccharide antigen (pneumococcal polysaccharide). In parallel, the proliferative Response of CD4+ T-cells to the Primary protein antigens keyhole limpet hemocyanin (KLH) and sperm whale myoglobin (SWM) was measured in vitro using monocyte-derived dendritic cells (MDDC) as antigen-presenting cells. Compared to healthy controls, type-1 diabetes patients mounted a significantly impaired Primary antibody Response to hepatitis A vaccine (median HAV antibody titer after the first vaccination, 53 IU/L in diabetic patients vs 212 IU/L in the controls, P = 0.017) and diphtheria toxoid (median serum antibodies after vaccination, patients, 0.94 IU/ml, controls, 6.38 IU/ml, P = 0.004), while the Response to pneumococcal polysaccharide was normal. Type-2 diabetes patients had a comparable metabolic dysregulation but showed a normal antibody Response following vaccination, demonstrating that the effect was not due to hyperglycemia. Antigen-induced interferon-gamma and interleukin-13 release was reduced in type-1 diabetes patients, localizing the impairment to the level of antigen-presenting cell-T-cell interaction. In addition, the proliferative Response of CD4+ T-cells derived from type-1 diabetes patients to KLH and SWM was significantly reduced (P < or = 0.01). FACS analysis of CD80 (B7.1), CD86 (B7.2), and HLA-DR expression on MDDC could not demonstrate significant differences in the expression of these molecules between type-1 and type-2 diabetes patients and healthy controls. An association of low HAV antibody Response with HLA-DR3,4 expression in the patients was shown. Our results indicate that the Primary antibody Response to T-cell dependent antigens as well as the T-cell Response to Primary protein antigens is reduced in type-1 diabetes patients and that additional booster immunization can overcome the defect.
Guntram Schernthaner - One of the best experts on this subject based on the ideXlab platform.
-
impaired Primary Immune Response in type 1 diabetes functional impairment at the level of apcs and t cells
Cellular Immunology, 2003Co-Authors: Martin Spatz, Nicole Eibl, Sandra Hink, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Martha M EiblAbstract:We have recently described an impaired proliferative Response of CD4(+) T-cells to Primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. Immunol. 103 (2002) 249]. In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the Immune Response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the Immune Response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the Primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. Taken together, our data suggest that a deviation in the expression of certain molecules known to be involved in the peripheral control of the Immune Response is present in IDDM patients and is underlying the observed impairment of the Primary Immune Response.
-
impaired Primary Immune Response in type 1 diabetes results from a controlled vaccination study
Clinical Immunology, 2002Co-Authors: Nicole Eibl, Martin Spatz, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Aysen Samstag, Martha M EiblAbstract:Patients with diabetes have an increased risk for infections, but information on their adoptive immunity is incomplete and contradictory. Twenty patients with diabetes type-1 and 20 patients with type-2 diabetes were vaccinated with T-cell-dependent Primary protein antigens (hepatitis A viral antigen, HAV; diphtheria toxoid) and a T-cell-independent polysaccharide antigen (pneumococcal polysaccharide). In parallel, the proliferative Response of CD4+ T-cells to the Primary protein antigens keyhole limpet hemocyanin (KLH) and sperm whale myoglobin (SWM) was measured in vitro using monocyte-derived dendritic cells (MDDC) as antigen-presenting cells. Compared to healthy controls, type-1 diabetes patients mounted a significantly impaired Primary antibody Response to hepatitis A vaccine (median HAV antibody titer after the first vaccination, 53 IU/L in diabetic patients vs 212 IU/L in the controls, P = 0.017) and diphtheria toxoid (median serum antibodies after vaccination, patients, 0.94 IU/ml, controls, 6.38 IU/ml, P = 0.004), while the Response to pneumococcal polysaccharide was normal. Type-2 diabetes patients had a comparable metabolic dysregulation but showed a normal antibody Response following vaccination, demonstrating that the effect was not due to hyperglycemia. Antigen-induced interferon-gamma and interleukin-13 release was reduced in type-1 diabetes patients, localizing the impairment to the level of antigen-presenting cell-T-cell interaction. In addition, the proliferative Response of CD4+ T-cells derived from type-1 diabetes patients to KLH and SWM was significantly reduced (P < or = 0.01). FACS analysis of CD80 (B7.1), CD86 (B7.2), and HLA-DR expression on MDDC could not demonstrate significant differences in the expression of these molecules between type-1 and type-2 diabetes patients and healthy controls. An association of low HAV antibody Response with HLA-DR3,4 expression in the patients was shown. Our results indicate that the Primary antibody Response to T-cell dependent antigens as well as the T-cell Response to Primary protein antigens is reduced in type-1 diabetes patients and that additional booster immunization can overcome the defect.
W R Mayr - One of the best experts on this subject based on the ideXlab platform.
-
impaired Primary Immune Response in type 1 diabetes functional impairment at the level of apcs and t cells
Cellular Immunology, 2003Co-Authors: Martin Spatz, Nicole Eibl, Sandra Hink, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Martha M EiblAbstract:We have recently described an impaired proliferative Response of CD4(+) T-cells to Primary antigens in patients with insulin-dependent diabetes mellitus (IDDM) [Clin. Immunol. 103 (2002) 249]. In order to further investigate possible mechanisms underlying this impairment, several factors known to be involved in the down-regulation of the Immune Response both at the level of APCs and CD4(+) T-cells were investigated: Monocyte-derived dendritic cells (MDDC) from IDDM patients were shown to express elevated amounts of CD86 (B7.2) (p=0.003) and reduced amounts of the adhesion molecule CD54 (ICAM-1) (p=0.03) on their cell surface compared to age-matched healthy controls and patients with non-insulin-dependent diabetes mellitus (NIDDM) as well as decreased SDS-PAGE stability of HLA-DQ and -DR peptide complexes directly isolated from the IDDM patients' peripheral blood mononuclear cells (PBMCs). Expression of CTLA-4 (CD152), known to be involved in the down-regulation of the Immune Response, was shown to be increased on CD4(+) T-cells from IDDM patients after exposure to the Primary antigen KLH (keyhole limpet hemocyanin) presented by MDDC (p=0.0047). Likewise, purified CD4(+) T-cells from IDDM patients produced elevated levels of the cytokine TGF-beta1 after stimulation with immobilized monoclonal antibodies directed against CD3 and CD28 (p=0.014). When monocytes from IDDM patients were stimulated with lipopolysaccharide (LPS), an increased tendency to produce the inhibitory cytokine interleukin (IL)-10 (p=0.007) and the acute phase cytokine IL-6 (p=0.044) was observed, whereas the concentrations of tumor necrosis factor (TNF)-alpha, IL-1beta, and IL-12 were comparable to controls. Taken together, our data suggest that a deviation in the expression of certain molecules known to be involved in the peripheral control of the Immune Response is present in IDDM patients and is underlying the observed impairment of the Primary Immune Response.
-
impaired Primary Immune Response in type 1 diabetes results from a controlled vaccination study
Clinical Immunology, 2002Co-Authors: Nicole Eibl, Martin Spatz, Hermann M Wolf, Gottfried Fischer, W R Mayr, Guntram Schernthaner, Aysen Samstag, Martha M EiblAbstract:Patients with diabetes have an increased risk for infections, but information on their adoptive immunity is incomplete and contradictory. Twenty patients with diabetes type-1 and 20 patients with type-2 diabetes were vaccinated with T-cell-dependent Primary protein antigens (hepatitis A viral antigen, HAV; diphtheria toxoid) and a T-cell-independent polysaccharide antigen (pneumococcal polysaccharide). In parallel, the proliferative Response of CD4+ T-cells to the Primary protein antigens keyhole limpet hemocyanin (KLH) and sperm whale myoglobin (SWM) was measured in vitro using monocyte-derived dendritic cells (MDDC) as antigen-presenting cells. Compared to healthy controls, type-1 diabetes patients mounted a significantly impaired Primary antibody Response to hepatitis A vaccine (median HAV antibody titer after the first vaccination, 53 IU/L in diabetic patients vs 212 IU/L in the controls, P = 0.017) and diphtheria toxoid (median serum antibodies after vaccination, patients, 0.94 IU/ml, controls, 6.38 IU/ml, P = 0.004), while the Response to pneumococcal polysaccharide was normal. Type-2 diabetes patients had a comparable metabolic dysregulation but showed a normal antibody Response following vaccination, demonstrating that the effect was not due to hyperglycemia. Antigen-induced interferon-gamma and interleukin-13 release was reduced in type-1 diabetes patients, localizing the impairment to the level of antigen-presenting cell-T-cell interaction. In addition, the proliferative Response of CD4+ T-cells derived from type-1 diabetes patients to KLH and SWM was significantly reduced (P < or = 0.01). FACS analysis of CD80 (B7.1), CD86 (B7.2), and HLA-DR expression on MDDC could not demonstrate significant differences in the expression of these molecules between type-1 and type-2 diabetes patients and healthy controls. An association of low HAV antibody Response with HLA-DR3,4 expression in the patients was shown. Our results indicate that the Primary antibody Response to T-cell dependent antigens as well as the T-cell Response to Primary protein antigens is reduced in type-1 diabetes patients and that additional booster immunization can overcome the defect.
