Background: The autoimmune disease type 1 diabetes mellitus (T1D) is associated with a defect in the immune response, which increases susceptibility to infection. We recently demonstrated that prolonged elevated levels of type 1 interferon (IFN) induce lymphocyte exhaustion during T1D. Aims: In the present study, we further investigated the effect of blocking the type I IFN receptor signaling pathway on diabetic dyslipidemia, in which an abnormal lipid profile leads to the exhaustion of B cells and alteration of their distribution and functions. Methods: T1D was induced in a mouse model by an intraperitoneal injection of a single dose (60 mg/kg) of streptozotocin (STZ). Three groups of mice were examined: a non-diabetic control group, a diabetic group and a diabetic group treated with an anti-IFN (alpha, beta and omega) receptor 1 (IFNAR1) blocking antibody to block type I IFN signaling. Results: We observed that induction of T1D was accompanied by a marked destruction of β cells and a reduction in the insulin levels in the diabetic group. Diabetic mice exhibited many changes, including alterations in their lipid profiles, expansion of splenic B cells, increased caspase-3, -8 and -9 activity, and apoptosis in peripheral B cells. Blocking type 1 IFN signaling in diabetic mice significantly returned the insulin and lipid profiles to normal levels, subsequently restored the B cell distribution, and rescued the peripheral B cells from apoptosis. Conclusion: Our data suggest the potential role of type I IFN in mediating diabetic dyslipidemia and an exhausted state of B cells during T1D.

BACKGROUND: The autoimmune disease type 1 diabetes mellitus (T1D) is associated with a defect in the immune response, which increases susceptibility to infection. We recently demonstrated that prolonged elevated levels of type 1 interferon (IFN) induce lymphocyte exhaustion during T1D. AIMS: In the present study, we further investigated the effect of blocking the type I IFN receptor signaling pathway on diabetic dyslipidemia, in which an abnormal lipid profile leads to the exhaustion of B cells and alteration of their distribution and functions. METHODS: T1D was induced in a mouse model by an intraperitoneal injection of a single dose (60 mg/kg) of streptozotocin (STZ). Three groups of mice were examined: a non-diabetic control group, a diabetic group and a diabetic group treated with an anti-IFN (alpha, beta and omega) receptor 1 (IFNAR1) blocking antibody to block type I IFN signaling. RESULTS: We observed that induction of T1D was accompanied by a marked destruction of β cells and a reduction in the insulin levels in the diabetic group. Diabetic mice exhibited many changes, including alterations in their lipid profiles, expansion of splenic B cells, increased caspase-3, -8 and -9 activity, and apoptosis in peripheral B cells. Blocking type 1 IFN signaling in diabetic mice significantly returned the insulin and lipid profiles to normal levels, subsequently restored the B cell distribution, and rescued the peripheral B cells from apoptosis. CONCLUSION: Our data suggest the potential role of type I IFN in mediating diabetic dyslipidemia and an exhausted state of B cells during T1D.

Background: The autoimmune disease type 1 diabetes mellitus (T1D) is associated with a defect in the immune response, which increases susceptibility to infection. We recently demonstrated that prolonged elevated levels of type 1 interferon (IFN) induce lymphocyte exhaustion during T1D. Aims: In the present study, we further investigated the effect of blocking the type I IFN receptor signaling pathway on diabetic dyslipidemia, in which an abnormal lipid profile leads to the exhaustion of B cells and alteration of their distribution and functions. Methods: T1D was induced in a mouse model by an intraperitoneal injection of a single dose (60 mg/kg) of streptozotocin (STZ). Three groups of mice were examined: a non-diabetic control group, a diabetic group and a diabetic group treated with an anti-IFN (alpha, beta and omega) receptor 1 (IFNAR1) blocking antibody to block type I IFN signaling. Results: We observed that induction of T1D was accompanied by a marked destruction of β cells and a reduction in the insulin levels in the diabetic group. Diabetic mice exhibited many changes, including alterations in their lipid profiles, expansion of splenic B cells, increased caspase-3, -8 and -9 activity, and apoptosis in peripheral B cells. Blocking type 1 IFN signaling in diabetic mice significantly returned the insulin and lipid profiles to normal levels, subsequently restored the B cell distribution, and rescued the peripheral B cells from apoptosis. Conclusion: Our data suggest the potential role of type I IFN in mediating diabetic dyslipidemia and an exhausted state of B cells during T1D.

Angular distributions of 16O + 16O elastic scattering at energies that range from 124 to 1120 MeV have been analyzed in the framework of the double folding (DF) optical model. Based upon the α-cluster structure of the 16O nucleus, two different versions of the real DF optical potential have been generated by using three effective α-α, α-nucleon (N) and nucleon-nucleon (NN) interactions. A microscopic optical potential built upon the M3Y effective NN interaction and the matter density distribution of the 16O nucleus has also been extracted. The obtained real potentials, in conjunction with phenomenological squaredWoods-Saxon imaginary parts, have successfully reproduced seven sets of elastic-scattering data. No renormalization of the real folded α-cluster potentials is required to fit the data. The energy dependence of the extracted real and imaginary volume integrals and total reaction cross section has also been investigated.

Angular distributions of 16O + 16O elastic scattering at energies that range from 124 to 1120 MeV have been analyzed in the framework of the double folding (DF) optical model. Based upon the α-cluster structure of the 16O nucleus, two different versions of the real DF optical potential have been generated by using three effective α-α, α-nucleon (N) and nucleon-nucleon (NN) interactions. A microscopic optical potential built upon the M3Y effective NN interaction and the matter density distribution of the 16O nucleus has also been extracted. The obtained real potentials, in conjunction with phenomenological squaredWoods-Saxon imaginary parts, have successfully reproduced seven sets of elastic-scattering data. No renormalization of the real folded α-cluster potentials is required to fit the data. The energy dependence of the extracted real and imaginary volume integrals and total reaction cross section has also been investigated.

The elastic scattering of 6,7Li+28Si reactions has been analyzed in the framework of the double folding optical model. Semi-microscopic folded potentials are generated based on the alpha (α)-cluster structure of the colliding nuclei. Successful reproduction of the observed angular distributions of the elastic scattering differential cross section and reaction cross sections has been obtained at different energies using the derived potentials. A microscopic folding approach based on the effective DDM3Y nucleon–nucleon interaction and the nuclear matter densities of the interacting nuclei is also considered.

The vector analyzing power and differential cross-section for the elastic scattering of 8He nucleus from polarized protons at 71MeV/nucleon have been analyzed in the framework of the optical model potentials. Microscopic single folding (SF) optical potentials (OP) have been constructed based upon two different effective nucleon–nucleon (NN) interactions, namely Jeukenne–Lejeune–Mahaux (JLM) and BDM3Y1 effective interactions. The effect of 8He nuclear structure has been tested through two different choices of the nuclear density distribution. It is concluded that the nucleus 8He may be considered as a thick skin exotic nucleus. In order to investigate the vector analyzing power data, besides the Thomas phenomenological representation, three different forms of the spin–orbit (SO) part of the OP have been considered. These forms are based directly or indirectly upon the density distribution of 8He nucleus. It is found that SO potentials of larger root mean square radii are able to successfully describe the vector analyzing power data more than those of shorter radii.