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1.
J Pediatr Endocrinol Metab ; 35(3): 393-397, 2022 Mar 28.
Article in English | MEDLINE | ID: covidwho-1622388

ABSTRACT

OBJECTIVES: It has been hypothesized that SARS-CoV-2 may play a role in the development of different forms of diabetes mellitus (DM). The Canary Islands have the highest incidence of type 1 DM (T1DM) reported in Spain (30-35/100,000 children under 14 years/year). In 2020-2021 we observed the highest incidence so far on the island of Gran Canaria, as a result of which we decided to evaluate the possible role of COVID-19 in the increased number of onsets. METHODS: We examined the presence of IgG antibodies against SARS-CoV-2 in children with new onset T1DM between October 2020 and August 2021. We compared recent T1DM incidence with that of the previous 10 years. RESULTS: Forty-two patients were diagnosed with T1DM (48.1/100,000 patients/year), representing a nonsignificant 25.7% increase from the expected incidence. Of the 33 patients who consented to the study, 32 presented negative IgG values, with only one patient reflecting undiagnosed past infection. Forty-four percent of patients presented with ketoacidosis at onset, which was similar to previous years. CONCLUSIONS: We conclude that there is no direct relationship between the increased incidence of T1DM and SARS-CoV-2 in the region. The COVID-19 pandemic did not result in an increased severity of T1DM presentation.


Subject(s)
Antibodies, Viral/blood , COVID-19/epidemiology , Diabetes Mellitus, Type 1/epidemiology , Diabetes Mellitus, Type 1/virology , SARS-CoV-2/immunology , Adolescent , Autoantibodies/blood , Child , Child, Preschool , Diabetes Mellitus, Type 1/immunology , Diabetic Ketoacidosis/epidemiology , Humans , Immunoglobulin G/blood , Infant , Infant, Newborn , Islets of Langerhans/immunology , Spain/epidemiology
2.
J Steroid Biochem Mol Biol ; 213: 105957, 2021 10.
Article in English | MEDLINE | ID: covidwho-1561628

ABSTRACT

This review examines the beneficial effects of ultraviolet radiation on systemic autoimmune diseases, including multiple sclerosis and type I diabetes, where the epidemiological evidence for the vitamin D-independent effects of sunlight is most apparent. Ultraviolet radiation, in addition to its role in the synthesis of vitamin D, stimulates anti-inflammatory pathways, alters the composition of dendritic cells, T cells, and T regulatory cells, and induces nitric oxide synthase and heme oxygenase metabolic pathways, which may directly or indirectly mitigate disease progression and susceptibility. Recent work has also explored how the immune-modulating functions of ultraviolet radiation affect type II diabetes, cancer, and the current global pandemic caused by SARS-CoV-2. These diseases are particularly important amidst global changes in lifestyle that result in unhealthy eating, increased sedentary habits, and alcohol and tobacco consumption. Compelling epidemiological data shows increased ultraviolet radiation associated with reduced rates of certain cancers, such as colorectal cancer, breast cancer, non-Hodgkins lymphoma, and ultraviolet radiation exposure correlated with susceptibility and mortality rates of COVID-19. Therefore, understanding the effects of ultraviolet radiation on both vitamin D-dependent and -independent pathways is necessary to understand how they influence the course of many human diseases.


Subject(s)
COVID-19/prevention & control , Diabetes Mellitus, Type 1/prevention & control , Diabetes Mellitus, Type 2/prevention & control , Multiple Sclerosis/prevention & control , Neoplasms/prevention & control , Sunlight , Vitamin D/metabolism , Alcohol Drinking/adverse effects , COVID-19/immunology , COVID-19/pathology , COVID-19/virology , Dendritic Cells/immunology , Dendritic Cells/radiation effects , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/pathology , Diabetes Mellitus, Type 2/immunology , Diabetes Mellitus, Type 2/pathology , Disease Progression , Disease Susceptibility , Heme Oxygenase (Decyclizing)/genetics , Heme Oxygenase (Decyclizing)/immunology , Humans , Multiple Sclerosis/immunology , Multiple Sclerosis/pathology , Neoplasms/immunology , Neoplasms/pathology , Nitric Oxide Synthase/genetics , Nitric Oxide Synthase/immunology , SARS-CoV-2/pathogenicity , SARS-CoV-2/radiation effects , Sedentary Behavior , T-Lymphocytes/immunology , T-Lymphocytes/radiation effects , Vitamin D/immunology
4.
Diabetes Metab Res Rev ; 38(1): e3505, 2022 01.
Article in English | MEDLINE | ID: covidwho-1469447

ABSTRACT

Multiple sclerosis (MS) and type 1 diabetes (T1D) are chronic conditions that result from dysfunction of the immune system. Their common root in autoimmunity stimulates interest in the exploration of similarities and differences between the two diseases. Genetic susceptibility is relevant, creating a substrate, on which environmental factors act as a trigger of an aberrant immune response. Despite being both T-cell mediated disorders with a strong involvement of the humoral arm, immunomodulation is a mainstay of MS management, whereas hormone replacement therapy remains the principal approach for T1D. T1D is usually diagnosed in children and adolescents, while MS is typical of young adults. This difference has implications for disease progression and treatment. The SARS-CoV-2 pandemic and its effect on immunity may affect the prevalence of these conditions, as well as their clinical manifestation.


Subject(s)
Diabetes Mellitus, Type 1 , Multiple Sclerosis , COVID-19/epidemiology , COVID-19/immunology , Diabetes Mellitus, Type 1/epidemiology , Diabetes Mellitus, Type 1/immunology , Humans , Multiple Sclerosis/epidemiology , Multiple Sclerosis/immunology , Pandemics
5.
J Clin Invest ; 131(11)2021 06 01.
Article in English | MEDLINE | ID: covidwho-1448082

ABSTRACT

First administered to a human subject as a tuberculosis (TB) vaccine on July 18, 1921, Bacillus Calmette-Guérin (BCG) has a long history of use for the prevention of TB and later the immunotherapy of bladder cancer. For TB prevention, BCG is given to infants born globally across over 180 countries and has been in use since the late 1920s. With about 352 million BCG doses procured annually and tens of billions of doses having been administered over the past century, it is estimated to be the most widely used vaccine in human history. While its roles for TB prevention and bladder cancer immunotherapy are widely appreciated, over the past century, BCG has been also studied for nontraditional purposes, which include (a) prevention of viral infections and nontuberculous mycobacterial infections, (b) cancer immunotherapy aside from bladder cancer, and (c) immunologic diseases, including multiple sclerosis, type 1 diabetes, and atopic diseases. The basis for these heterologous effects lies in the ability of BCG to alter immunologic set points via heterologous T cell immunity, as well as epigenetic and metabolomic changes in innate immune cells, a process called "trained immunity." In this Review, we provide an overview of what is known regarding the trained immunity mechanism of heterologous protection, and we describe the current knowledge base for these nontraditional uses of BCG.


Subject(s)
Diabetes Mellitus, Type 1/therapy , Immunity, Cellular , Multiple Sclerosis/therapy , Mycobacterium bovis/immunology , T-Lymphocytes/immunology , Urinary Bladder Neoplasms/therapy , Virus Diseases/therapy , Animals , Diabetes Mellitus, Type 1/history , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/pathology , History, 20th Century , History, 21st Century , Humans , Multiple Sclerosis/history , Multiple Sclerosis/immunology , Multiple Sclerosis/pathology , Mycobacterium Infections, Nontuberculous/history , Mycobacterium Infections, Nontuberculous/immunology , Mycobacterium Infections, Nontuberculous/pathology , Mycobacterium Infections, Nontuberculous/prevention & control , Tuberculosis/history , Tuberculosis/immunology , Tuberculosis/prevention & control , Urinary Bladder Neoplasms/history , Urinary Bladder Neoplasms/immunology , Urinary Bladder Neoplasms/pathology , Virus Diseases/history , Virus Diseases/immunology , Virus Diseases/pathology
6.
Front Immunol ; 12: 722979, 2021.
Article in English | MEDLINE | ID: covidwho-1399139

ABSTRACT

The immunopathology of type I diabetes (T1D) presents a complicated case in part because of the multifactorial origin of this disease. Typically, T1D is thought to occur as a result of autoimmunity toward islets of Langerhans, resulting in the destruction of insulin-producing cells (ß cells) and thus lifelong reliance on exogenous insulin. However, that explanation obscures much of the underlying mechanism, and the actual precipitating events along with the associated actors (latent viral infection, diverse immune cell types and their roles) are not completely understood. Notably, there is a malfunctioning in the regulation of cytotoxic CD8+ T cells that target endocrine cells through antigen-mediated attack. Further examination has revealed the likelihood of an imbalance in distinct subpopulations of tolerogenic and cytotoxic natural killer (NK) cells that may be the catalyst of adaptive immune system malfunction. The contributions of components outside the immune system, including environmental factors such as chronic viral infection also need more consideration, and much of the recent literature investigating the origins of this disease have focused on these factors. In this review, the details of the immunopathology of T1D regarding NK cell disfunction is discussed, along with how those mechanisms stand within the context of general autoimmune disorders. Finally, the rarer cases of latent autoimmune, COVID-19 (viral), and immune checkpoint inhibitor (ICI) induced diabetes are discussed as their exceptional pathology offers insight into the evolution of the disease as a whole.


Subject(s)
Autoimmune Diseases/immunology , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/pathology , Killer Cells, Natural/immunology , Killer Cells, Natural/pathology , Autoantibodies/immunology , Autoimmune Diseases/pathology , COVID-19/complications , Diabetes Mellitus, Type 1/etiology , Humans , Insulin/metabolism , Insulin-Secreting Cells/immunology , Virus Diseases/complications
7.
Front Immunol ; 12: 730414, 2021.
Article in English | MEDLINE | ID: covidwho-1376703

ABSTRACT

Antigen-specific immunotherapy (ASI) holds great promise for type 1 diabetes (T1D). Preclinical success for this approach has been demonstrated in vivo, however, clinical translation is still pending. Reasons explaining the slow progress to approve ASI are complex and span all stages of research and development, in both academic and industry environments. The basic four hurdles comprise a lack of translatability of pre-clinical research to human trials; an absence of robust prognostic and predictive biomarkers for therapeutic outcome; a need for a clear regulatory path addressing ASI modalities; and the limited acceptance to develop therapies intervening at the pre-symptomatic stages of disease. The core theme to address these challenges is collaboration-early, transparent, and engaged interactions between academic labs, pharmaceutical research and clinical development teams, advocacy groups, and regulatory agencies to drive a fundamental shift in how we think and treat T1D.


Subject(s)
Antigens/immunology , Autoimmunity , Diabetes Mellitus, Type 1/therapy , Immunotherapy , Animals , Biomarkers/metabolism , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/metabolism , Humans , Immunotherapy/adverse effects
8.
Front Immunol ; 12: 702506, 2021.
Article in English | MEDLINE | ID: covidwho-1376698

ABSTRACT

Type 1 diabetes (T1D) is a proinflammatory pathology that leads to the specific destruction of insulin producing ß-cells and hyperglycaemia. Much of the knowledge about type 1 diabetes (T1D) has focused on mechanisms of disease progression such as adaptive immune cells and the cytokines that control their function, whereas mechanisms linked with the initiation of the disease remain unknown. It has been hypothesized that in addition to genetics, environmental factors play a pivotal role in triggering ß-cell autoimmunity. The BioBreeding Diabetes Resistant (BBDR) and LEW1.WR1 rats have been used to decipher the mechanisms that lead to virus-induced T1D. Both animals develop ß-cell inflammation and hyperglycemia upon infection with the parvovirus Kilham Rat Virus (KRV). Our earlier in vitro and in vivo studies indicated that KRV-induced innate immune upregulation early in the disease course plays a causal role in triggering ß-cell inflammation and destruction. Furthermore, we recently found for the first time that infection with KRV induces inflammation in visceral adipose tissue (VAT) detectable as early as day 1 post-infection prior to insulitis and hyperglycemia. The proinflammatory response in VAT is associated with macrophage recruitment, proinflammatory cytokine and chemokine upregulation, endoplasmic reticulum (ER) and oxidative stress responses, apoptosis, and downregulation of adipokines and molecules that mediate insulin signaling. Downregulation of inflammation suppresses VAT inflammation and T1D development. These observations are strikingly reminiscent of data from obesity and type 2 diabetes (T2D) in which VAT inflammation is believed to play a causal role in disease mechanisms. We propose that VAT inflammation and dysfunction may be linked with the mechanism of T1D progression.


Subject(s)
Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/virology , Intra-Abdominal Fat/immunology , Intra-Abdominal Fat/virology , Parvoviridae Infections/immunology , Animals , Humans , Parvovirus/immunology , Rats
10.
J Pediatr Endocrinol Metab ; 34(10): 1303-1309, 2021 Oct 26.
Article in English | MEDLINE | ID: covidwho-1320552

ABSTRACT

OBJECTIVES: The COVID-19 pandemic is a global health problem with high morbidity and mortality. This study aimed to investigate patients who were diagnosed with type 1 diabetes during the pandemic and evaluate the effect of the pandemic on the clinical findings of these patients by comparing them with findings from a year prior. METHODS: Patients diagnosed with type 1 diabetes mellitus between 2019 and 2021 were separated into two groups: Patients diagnosed prepandemic and those diagnosed during the pandemic. RESULTS: The number of newly diagnosed diabetes cases increased from 46 in the prepandemic period to 74 in the pandemic period. The number of cases diagnosed with diabetic ketoacidosis (DKA) in the clinic increased from 58.7 to 91.9%. We found that moderate and severe DKA rates from 18.5 and 14.8% to 23.5 and 22.1%, respectively. Besides, the average HbA1c was higher, while the average bicarbonate was lower in cases diagnosed during the pandemic period compared to the prepandemic period (p=0.048 and p<0.001, respectively). We found that celiac autoantibody positivity antibodies to glutamic acid decarboxylase (anti GAD) positivity, and islet cell antibodies (ICA), ICA and anti GAD positivity coexistence were higher (p=0.045, p=0.008, and p=0.007, respectively) among the patients diagnosed during the pandemic. CONCLUSIONS: We observed an increase in the number of patients newly diagnosed with type 1 diabetes mellitus, an increase in autoantibody positivity, and higher rates and severity of DKA during the COVID-19 pandemic period compared to the prepandemic period.


Subject(s)
COVID-19/epidemiology , Diabetes Mellitus, Type 1/epidemiology , SARS-CoV-2 , Adolescent , Autoantibodies/analysis , Child , Child, Preschool , Cross-Sectional Studies , Diabetes Mellitus, Type 1/immunology , Diabetic Ketoacidosis/epidemiology , Humans , Infant , Male , Tertiary Care Centers , Turkey/epidemiology
11.
J Pediatr Endocrinol Metab ; 34(10): 1319-1322, 2021 Oct 26.
Article in English | MEDLINE | ID: covidwho-1317154

ABSTRACT

OBJECTIVES: Questions are emerging concerning the long-term consequences of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, as a possible increase in type 1 diabetes. This study aims to describe the prevalence of anti-SARS-CoV-2 antibodies in children developing type 1 diabetes during this pandemic in Belgium. METHODS: This observational study included children and adolescents (under 16 years) admitted with new-onset type 1 diabetes. SARS-CoV-2 serology was taken within the first month of diabetes. RESULTS: Of the 75 participants, anti-SARS-CoV-2 antibodies were positive in 20% of patients. They had an increased bicarbonate and base excess at diagnosis. Overall 29% of patients presented diabetic ketoacidosis at diagnosis and 9% of them were positive for anti-SARS-CoV-2 antibodies. Insulinoma-associated protein 2 antibodies positivity had significantly higher frequencies in children without anti-SARS-CoV-2 antibodies (49 (81%) vs. 5 (33%), p=0.038). Nine (15%) patients, initially seronegative, have developed anti-SARS-CoV-2 antibodies between the two samples (mean time 8 ± 4 weeks). CONCLUSIONS: The prevalence of anti-SARS-CoV-2 antibodies in children with newly diagnosed type 1 diabetes (20%) is similar to that found in children without diabetes in Belgium, a country severely affected by this pandemic.


Subject(s)
Antibodies, Viral/blood , COVID-19/epidemiology , Diabetes Mellitus, Type 1/immunology , SARS-CoV-2/immunology , Adolescent , Belgium/epidemiology , Child , Child, Preschool , Female , Humans , Male
13.
Front Immunol ; 12: 678771, 2021.
Article in English | MEDLINE | ID: covidwho-1278395

ABSTRACT

Chronic and recurrent infections occur commonly in both type 1 and type 2 diabetes (T1D, T2D) and increase patient morbidity and mortality. Neutrophils are professional phagocytes of the innate immune system that are critical in pathogen handling. Neutrophil responses to infection are dysregulated in diabetes, predominantly mediated by persistent hyperglycaemia; the chief biochemical abnormality in T1D and T2D. Therapeutically enhancing host immunity in diabetes to improve infection resolution is an expanding area of research. Individuals with diabetes are also at an increased risk of severe coronavirus disease 2019 (COVID-19), highlighting the need for re-invigorated and urgent focus on this field. The aim of this review is to explore the breadth of previous literature investigating neutrophil function in both T1D and T2D, in order to understand the complex neutrophil phenotype present in this disease and also to focus on the development of new therapies to improve aberrant neutrophil function in diabetes. Existing literature illustrates a dual neutrophil dysfunction in diabetes. Key pathogen handling mechanisms of neutrophil recruitment, chemotaxis, phagocytosis and intracellular reactive oxygen species (ROS) production are decreased in diabetes, weakening the immune response to infection. However, pro-inflammatory neutrophil pathways, mainly neutrophil extracellular trap (NET) formation, extracellular ROS generation and pro-inflammatory cytokine generation, are significantly upregulated, causing damage to the host and perpetuating inflammation. Reducing these proinflammatory outputs therapeutically is emerging as a credible strategy to improve infection resolution in diabetes, and also more recently COVID-19. Future research needs to drive forward the exploration of novel treatments to improve infection resolution in T1D and T2D to improve patient morbidity and mortality.


Subject(s)
Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 2/immunology , Inflammation/immunology , Neutrophils/immunology , COVID-19/immunology , Humans , SARS-CoV-2
14.
Immunology ; 164(3): 467-475, 2021 11.
Article in English | MEDLINE | ID: covidwho-1266332

ABSTRACT

A number of mechanisms have been proposed to explain the well-established link between diabetic status and an increased susceptibility to infection. Notably, diabetes has been shown to be one of the strongest factors influencing healthcare outcome in COVID-19 infections. Though it has long been noted that lymphocytes upregulate insulin receptors following immune activation, until recently, this observation has received little attention. Here, we point out key findings implicating dysregulated insulin signalling in immune cells as a possible contributing factor in the immune pathology associated with diabetes. Mechanistically, insulin, by activating the PI3K/Akt/mTOR pathway, regulates various aspects of both myeloid cells and lymphocytes, such as cell survival, metabolic reprogramming and the polarization and differentiation of immune cells. PI3K signalling is also supressed by immune checkpoint proteins, suggesting that insulin signalling may antagonize peripheral tolerance. Remarkably, it has also recently been shown that, following insulin binding, the insulin receptor translocates to the nucleus where it plays a key role in regulating the transcription of various immune-related genes, including pathways involved in viral infections. Taken together, these observations suggest that dysregulated insulin signalling may directly contribute to a defective immune response during COVID-19 infections.


Subject(s)
Blood Glucose/metabolism , COVID-19/metabolism , Diabetes Mellitus, Type 1/metabolism , Insulin/metabolism , Lymphocytes/metabolism , SARS-CoV-2/pathogenicity , Animals , Biomarkers/blood , COVID-19/immunology , COVID-19/physiopathology , COVID-19/virology , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/physiopathology , Host-Pathogen Interactions , Humans , Immune Checkpoint Proteins/metabolism , Insulin Resistance , Lymphocytes/immunology , Lymphocytes/virology , Phosphatidylinositol 3-Kinase/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Receptor, Insulin/metabolism , SARS-CoV-2/immunology , SARS-CoV-2/metabolism , Signal Transduction , TOR Serine-Threonine Kinases/metabolism
15.
Arch Dis Child ; 107(2): 180-185, 2022 02.
Article in English | MEDLINE | ID: covidwho-1247330

ABSTRACT

BACKGROUND: Viral infections may trigger type 1 diabetes (T1D), and recent reports suggest an increased incidence of paediatric T1D and/or diabetic ketoacidosis (DKA) during the COVID-19 pandemic. OBJECTIVE: To study whether the number of children admitted to the paediatric intensive care unit (PICU) for DKA due to new-onset T1D increased during the COVID-19 pandemic, and whether SARS-CoV-2 infection plays a role. METHODS: This retrospective cohort study comprises two datasets: (1) children admitted to PICU due to new-onset T1D and (2) children diagnosed with new-onset T1D and registered to the Finnish Pediatric Diabetes Registry in the Helsinki University Hospital from 1 April to 31 October in 2016-2020. We compared the incidence, number and characteristics of children with newly diagnosed T1D between the prepandemic and pandemic periods. RESULTS: The number of children admitted to PICU due to new-onset T1D increased from an average of 6.25 admissions in 2016-2019 to 20 admissions in 2020 (incidence rate ratio [IRR] 3.24 [95% CI 1.80 to 5.83]; p=0.0001). On average, 57.75 children were registered to the FPDR in 2016-2019, as compared with 84 in 2020 (IRR 1.45; 95% CI 1.13 to 1.86; p=0.004). 33 of the children diagnosed in 2020 were analysed for SARS-CoV-2 antibodies, and all were negative. CONCLUSIONS: More children with T1D had severe DKA at diagnosis during the pandemic. This was not a consequence of SARS-CoV-2 infection. Instead, it probably stems from delays in diagnosis following changes in parental behaviour and healthcare accessibility.


Subject(s)
COVID-19/epidemiology , Diabetes Mellitus, Type 1/epidemiology , Diabetic Ketoacidosis/epidemiology , Adolescent , COVID-19/complications , COVID-19/immunology , COVID-19/virology , Child , Child, Preschool , Communicable Disease Control/standards , Delayed Diagnosis/statistics & numerical data , Diabetes Mellitus, Type 1/diagnosis , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 1/therapy , Diabetic Ketoacidosis/diagnosis , Diabetic Ketoacidosis/immunology , Diabetic Ketoacidosis/therapy , Female , Finland/epidemiology , Health Services Accessibility/standards , Health Services Accessibility/statistics & numerical data , Humans , Incidence , Intensive Care Units, Pediatric/statistics & numerical data , Male , Pandemics/prevention & control , Pandemics/statistics & numerical data , Patient Admission/statistics & numerical data , Registries/statistics & numerical data , Retrospective Studies , SARS-CoV-2/immunology , Severity of Illness Index
16.
Front Immunol ; 12: 653974, 2021.
Article in English | MEDLINE | ID: covidwho-1202332

ABSTRACT

This study discusses substantive advances in T cell proliferation analysis, with the aim to provoke a re-evaluation of the generally-held view that Ki-67 is a reliable proliferation marker per se, and to offer a more sensitive and effective method for T cell cycle analysis, with informative examples in mouse and human settings. We summarize recent experimental work from our labs showing that, by Ki-67/DNA dual staining and refined flow cytometric methods, we were able to identify T cells in the S-G2/M phases of the cell-cycle in the peripheral blood (collectively termed "T Double S" for T cells in S-phase in Sanguine: in short "TDS" cells). Without our refinement, such cells may be excluded from conventional lymphocyte analyses. Specifically, we analyzed clonal expansion of antigen-specific CD8 T cells in vaccinated mice, and demonstrated the potential of TDS cells to reflect immune dynamics in human blood samples from healthy donors, and patients with type 1 diabetes, infectious mononucleosis, and COVID-19. The Ki-67/DNA dual staining, or TDS assay, provides a reliable approach by which human peripheral blood can be used to reflect the dynamics of human lymphocytes, rather than providing mere steady-state phenotypic snapshots. The method does not require highly sophisticated "-omics" capabilities, so it should be widely-applicable to health care in diverse settings. Furthermore, our results argue that the TDS assay can provide a window on immune dynamics in extra-lymphoid tissues, a long-sought potential of peripheral blood monitoring, for example in relation to organ-specific autoimmune diseases and infections, and cancer immunotherapy.


Subject(s)
CD8-Positive T-Lymphocytes/immunology , COVID-19/immunology , Cell Cycle/immunology , Diabetes Mellitus, Type 1/immunology , Ki-67 Antigen/immunology , Neoplasms/immunology , SARS-CoV-2/immunology , Animals , CD8-Positive T-Lymphocytes/pathology , COVID-19/pathology , COVID-19/prevention & control , COVID-19 Vaccines/immunology , COVID-19 Vaccines/therapeutic use , Diabetes Mellitus, Type 1/pathology , Diabetes Mellitus, Type 1/therapy , Humans , Mice , Neoplasms/pathology , Neoplasms/therapy
17.
Eur Rev Med Pharmacol Sci ; 24(21): 11409-11420, 2020 11.
Article in English | MEDLINE | ID: covidwho-937848

ABSTRACT

OBJECTIVE: Diabetes is a lifestyle disease and it has become an epidemic worldwide in recent decades. In the ongoing COVID-19 pandemic situation, diabetes has become a serious health concern since large numbers of patients are vulnerable to die from the virus. Thus, diabetic patients affected by COVID-19 cause a major health crisis now. Reports show that large occurrence of diabetes makes it a serious comorbidity in COVID-19 patients. MATERIALS AND METHODS: It is crucial to understand how COVID-19 affects diabetes patients. This paper has reviewed published literature extensively to understand the pattern, importance, care, and medication. RESULTS: This review summarizes the association between COVID-19 and diabetes in terms of susceptibility for pneumonia and other diseases. It also discusses the harshness of COVID-19 with diabetes populations and immunological impacts. It further adds the ACE2 receptor role in diabetes with COVID-19 patients. CONCLUSIONS: Finally, this paper illustrates different types of diabetes management techniques, such as blood glucose management, self-management, mental health management, and therapeutic management. It also summarizes the current knowledge about diabetic patients with COVID-19 to fight this pandemic.


Subject(s)
Betacoronavirus/immunology , Coronavirus Infections/immunology , Diabetes Mellitus, Type 1/complications , Diabetes Mellitus, Type 2/complications , Disease Susceptibility/immunology , Pneumonia, Viral/immunology , Angiotensin-Converting Enzyme 2 , Betacoronavirus/metabolism , Betacoronavirus/pathogenicity , Blood Glucose/drug effects , Blood Glucose/metabolism , COVID-19 , Comorbidity , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Diabetes Mellitus, Type 1/drug therapy , Diabetes Mellitus, Type 1/epidemiology , Diabetes Mellitus, Type 1/immunology , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/epidemiology , Diabetes Mellitus, Type 2/immunology , Humans , Hypoglycemic Agents/administration & dosage , Pancreas/pathology , Pandemics/prevention & control , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/diagnosis , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , SARS-CoV-2 , Severity of Illness Index , Spike Glycoprotein, Coronavirus/metabolism , Virus Replication/immunology
18.
Paediatr Respir Rev ; 36: 57-64, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-935867

ABSTRACT

The Bacille Calmette Guérin (BCG) vaccine was developed over a century ago and has become one of the most used vaccines without undergoing a modern vaccine development life cycle. Despite this, the vaccine has protected many millions from severe and disseminated forms of tuberculosis (TB). In addition, BCG has cross-mycobacterial effects against non-tuberculous mycobacteria and off-target (also called non-specific or heterologous) effects against other infections and diseases. More recently, BCG's effects on innate immunity suggest it might improve the immune response against viral respiratory infections including SARS-CoV-2. New TB vaccines, developed over the last 30 years, show promise, particularly in prevention of progression to disease from TB infection in young adults. The role of BCG in the context of new TB vaccines remains uncertain as most participants included in trials have been previously BCG immunised. BCG replacement vaccines are in efficacy trials and these may also have off-target effects.


Subject(s)
Adjuvants, Immunologic/therapeutic use , BCG Vaccine/therapeutic use , Cross Protection/immunology , Immunity, Heterologous/immunology , Mycobacterium Infections, Nontuberculous/prevention & control , Tuberculosis Vaccines/therapeutic use , Tuberculosis/prevention & control , BCG Vaccine/immunology , Buruli Ulcer/microbiology , Buruli Ulcer/prevention & control , COVID-19/prevention & control , Diabetes Mellitus, Type 1/epidemiology , Diabetes Mellitus, Type 1/immunology , Humans , Hypersensitivity/epidemiology , Hypersensitivity/immunology , Infant , Infant Mortality , Leprosy/microbiology , Leprosy/prevention & control , Mycobacterium Infections, Nontuberculous/microbiology , Nontuberculous Mycobacteria/immunology , Respiratory Tract Infections/epidemiology , Respiratory Tract Infections/immunology , Tuberculosis Vaccines/immunology
20.
Nat Metab ; 2(10): 1021-1024, 2020 10.
Article in English | MEDLINE | ID: covidwho-744385

ABSTRACT

Here we report a case where the manifestations of insulin-dependent diabetes occurred following SARS-CoV-2 infection in a young individual in the absence of autoantibodies typical for type 1 diabetes mellitus. Specifically, a 19-year-old white male presented at our emergency department with diabetic ketoacidosis, C-peptide level of 0.62 µg l-1, blood glucose concentration of 30.6 mmol l-1 (552 mg dl-1) and haemoglobin A1c of 16.8%. The patient´s case history revealed probable COVID-19 infection 5-7 weeks before admission, based on a positive test for antibodies against SARS-CoV-2 proteins as determined by enzyme-linked immunosorbent assay. Interestingly, the patient carried a human leukocyte antigen genotype (HLA DR1-DR3-DQ2) considered to provide only a slightly elevated risk of developing autoimmune type 1 diabetes mellitus. However, as noted, no serum autoantibodies were observed against islet cells, glutamic acid decarboxylase, tyrosine phosphatase, insulin and zinc-transporter 8. Although our report cannot fully establish causality between COVID-19 and the development of diabetes in this patient, considering that SARS-CoV-2 entry receptors, including angiotensin-converting enzyme 2, are expressed on pancreatic ß-cells and, given the circumstances of this case, we suggest that SARS-CoV-2 infection, or COVID-19, might negatively affect pancreatic function, perhaps through direct cytolytic effects of the virus on ß-cells.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Coronavirus Infections/diagnosis , Diabetes Mellitus, Type 1/complications , Pneumonia, Viral/complications , Pneumonia, Viral/diagnosis , Antibodies, Viral/blood , Antibodies, Viral/immunology , Autoantibodies/blood , Autoantibodies/immunology , Betacoronavirus/immunology , Biomarkers , COVID-19 , Coronavirus Infections/immunology , Diabetes Mellitus, Type 1/diagnosis , Diabetes Mellitus, Type 1/genetics , Diabetes Mellitus, Type 1/immunology , HLA-D Antigens/genetics , HLA-D Antigens/immunology , Humans , Immunoglobulin M/immunology , Insulin/metabolism , Insulin-Secreting Cells/immunology , Insulin-Secreting Cells/metabolism , Islets of Langerhans/immunology , Male , Pandemics , Pneumonia, Viral/immunology , SARS-CoV-2 , Young Adult
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