Effector Memory CD8 + and CD4 + T Cell Immunity Associated with Metabolic Syndrome in Obese Children / 대한소아소화기영양학회지

Purpose@#We investigated the association of effector memory (EM) CD8 + T cell and CD4 + T cell immunity with metabolic syndrome (MS). @*Methods@#Surface and intracellular staining of peripheral blood mononuclear cells was performed. Anti-interleukin-7 receptor-alpha (IL-7Rα) and CX3CR1 antibodies were used to stain the subsets of EM CD8 + T cells, while anti-interferon-gamma (IFN-γ), interleukin-17 (IL-17), and forkhead box P3 (FOXP3) antibodies were used for CD4 + T cell subsets. @*Results@#Of the 47 obese children, 11 were female. Children with MS had significantly higher levels of serum insulin (34.8±13.8 vs. 16.4±6.3 μU/mL, p<0.001) and homeostasis model assessment of insulin resistance (8.9±4.1 vs. 3.9±1.5, p<0.001) than children without MS.Children with MS revealed significantly higher frequencies of IL-7Rα low CD8+ T cells (60.1 ±19.1% vs. 48.4±11.5%, p=0.047) and IL-7Rα low CX3CR1 + CD8 + T cells (53.8±20.1% vs. 41.5 ±11.9%, p=0.036) than children without MS. As the serum triglyceride levels increased, the frequency of IL-7Rα low CX3CR1 + and IL-7Rα high CX3CR1 – CD8 + T cells increased and decreased, respectively (r=0.335, p=0.014 and r=−0.350, p=0.010, respectively), in 47 children. However, no CD4 + T cell subset parameters were significantly different between children with and without MS. @*Conclusion@#In obese children with MS, the changes in immunity due to changes in EM CD8 + T cells might be related to the morbidity of obesity.

Effector Memory CD8 + and CD4 + T Cell Immunity Associated with Metabolic Syndrome in Obese Children / 대한소아소화기영양학회지

Purpose@#We investigated the association of effector memory (EM) CD8 + T cell and CD4 + T cell immunity with metabolic syndrome (MS). @*Methods@#Surface and intracellular staining of peripheral blood mononuclear cells was performed. Anti-interleukin-7 receptor-alpha (IL-7Rα) and CX3CR1 antibodies were used to stain the subsets of EM CD8 + T cells, while anti-interferon-gamma (IFN-γ), interleukin-17 (IL-17), and forkhead box P3 (FOXP3) antibodies were used for CD4 + T cell subsets. @*Results@#Of the 47 obese children, 11 were female. Children with MS had significantly higher levels of serum insulin (34.8±13.8 vs. 16.4±6.3 μU/mL, p<0.001) and homeostasis model assessment of insulin resistance (8.9±4.1 vs. 3.9±1.5, p<0.001) than children without MS.Children with MS revealed significantly higher frequencies of IL-7Rα low CD8+ T cells (60.1 ±19.1% vs. 48.4±11.5%, p=0.047) and IL-7Rα low CX3CR1 + CD8 + T cells (53.8±20.1% vs. 41.5 ±11.9%, p=0.036) than children without MS. As the serum triglyceride levels increased, the frequency of IL-7Rα low CX3CR1 + and IL-7Rα high CX3CR1 – CD8 + T cells increased and decreased, respectively (r=0.335, p=0.014 and r=−0.350, p=0.010, respectively), in 47 children. However, no CD4 + T cell subset parameters were significantly different between children with and without MS. @*Conclusion@#In obese children with MS, the changes in immunity due to changes in EM CD8 + T cells might be related to the morbidity of obesity.

Microbiota in T-cell homeostasis and inflammatory diseases

The etiology of disease pathogenesis can be largely explained by genetic variations and several types of environmental factors. In genetically disease-susceptible individuals, subsequent environmental triggers may induce disease development. The human body is colonized by complex commensal microbes that have co-evolved with the host immune system. With the adaptation to modern lifestyles, its composition has changed depending on host genetics, changes in diet, overuse of antibiotics against infection and elimination of natural enemies through the strengthening of sanitation. In particular, commensal microbiota is necessary in the development, induction and function of T cells to maintain host immune homeostasis. Alterations in the compositional diversity and abundance levels of microbiota, known as dysbiosis, can trigger several types of autoimmune and inflammatory diseases through the imbalance of T-cell subpopulations, such as Th1, Th2, Th17 and Treg cells. Recently, emerging evidence has identified that dysbiosis is involved in the progression of rheumatoid arthritis, type 1 and 2 diabetic mellitus, and asthma, together with dysregulated T-cell subpopulations. In this review, we will focus on understanding the complicated microbiota-T-cell axis between homeostatic and pathogenic conditions and elucidate important insights for the development of novel targets for disease therapy.

Surgical Results of Trabeculectomy and Ahmed Valve Implantation Following a Previous Failed Trabeculectomy in Primary Congenital Glaucoma Patients

PURPOSE: To compare the surgical results of trabeculectomy and Ahmed glaucoma valve implantation after a previous failed trabeculectomy. METHODS: A retrospective comparative case series review was performed on 31 eye surgeries in 20 patients with primary congenital glaucoma who underwent trabeculectomy or Ahmed glaucoma valve implantation after a previous failed trabeculectomy with mitomycin C. RESULTS: The preoperative mean intraocular pressure was 25.5 mmHg in the trabeculectomy group and 26.9 mmHg in the Ahmed glaucoma valve implantation group (p = 0.73). The 48-month postoperative mean intraocular pressure was 19.6 mmHg in the trabeculectomy group and 20.2 mmHg in the Ahmed glaucoma valve implantation group (p = 0.95). The 12-month trabeculectomy success rate was 69%, compared with 64% for Ahmed glaucoma valve implantation, and the 48-month success rates were 42% and 36% for trabeculectomy and valve implantation, respectively. The success rates following the entire follow-up period were not significantly different between the two groups (p > 0.05 by log rank test). Postoperative complications occurred in 25% of the trabeculectomy-operated eyes and 9% of the Ahmed-implanted eyes (p = 0.38). CONCLUSIONS: There was no significant difference in surgical outcome between the trabeculectomy and Ahmed glaucoma valve implantation groups, neither of which had favorable results. However, the trabeculectomy group demonstrated a higher prevalence of adverse complications such as post-operative endophthalmitis.

Retinal Nerve Fiber Layer Defect Associated with Astrocytic Hamartoma in a Patient with Tuberous Sclerosis

PURPOSE: To report the progression of an astrocytic hamartoma of the right optic nerve head as well as the retina, and the progression of retinal nerve fiber defect associated with astrocytic hamartoma in a patient with tuberous sclerosis. CASE SUMMARY: A 6-year-old boy with tuberous sclerosis and an astrocytic hamartoma of the right optic nerve head, which was found at the time of ophthalmologie examinations, was referred from the pediatric neurologist for evaluation of the vigabatrin-associated visual field changes. Fundus examination revealed 1/2 disc diameter (DD)-sized astrocytic hamartoma located at the margin of the superior part of the optic nerve. The retina of the left eye was normal. Eighteen months after the first visit, enlarged optic disc hamartoma of the right eye and newly onset retinal astrocytic hamartoma located approximately 1.5 DD inferior to the fovea of the left eye were found. Three years later, an increase in the size of the astrocytic hamartoma of the right optic nerve and development of retinal nerve fiber defects were observed. CONCLUSIONS: Astrocytic hamartoma in patients with tuberous sclerosis is usually stable without progression. However, in our patient, astrocytic hamartoma showed progression, and development of retinal nerve fiber defects occurred. Regular follow-up is necessary for astrocytic hamartoma in patients with tuberous sclerosis.

Vitamin C Is an Essential Factor on the Anti-viral Immune Responses through the Production of Interferon-alpha/beta at the Initial Stage of Influenza A Virus (H3N2) Infection

L-ascorbic acid (vitamin C) is one of the well-known anti-viral agents, especially to influenza virus. Since the in vivo anti-viral effect is still controversial, we investigated whether vitamin C could regulate influenza virus infection in vivo by using Gulo (-/-) mice, which cannot synthesize vitamin C like humans. First, we found that vitamin C-insufficient Gulo (-/-) mice expired within 1 week after intranasal inoculation of influenza virus (H3N2/Hongkong). Viral titers in the lung of vitamin C-insufficient Gulo (-/-) mice were definitely increased but production of anti-viral cytokine, interferon (IFN)-alpha/beta, was decreased. On the contrary, the infiltration of inflammatory cells into the lung and production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-alpha/beta, were increased in the lung. Taken together, vitamin C shows in vivo anti-viral immune responses at the early time of infection, especially against influenza virus, through increased production of IFN-alpha/beta.