Clinical Immunology Communications最新文献

IL-10 receptor (IL-10R) deficiency is a rare immune dysregulation disorder that is characterized by early-onset and life-threatening inflammatory bowel disease (IBD). Activation of the IL-10R inhibits the release of pro-inflammatory cytokines resulting in decreased inflammation. Herein, we present a case of novel homozygous IL-10RA mutation (c.243T>A; p.Y81*) resulting in early-onset Crohn's disease and failure to thrive who was treated with anakinra (IL-1 blocker). His disease course was complicated with IgA nephropathy while anakinra was held for the treatment of osteomyelitis and improved when anakinra was restarted. A year later, he developed inflammatory brain disease and Hemophagocytic Lymphohistiocytosis (HLH), which was treated with high dose steroid and hematopoietic stem cell transplant (HSCT). This case highlights IgA nephropathy, CNS autoinflammation, and HLH as possible extraintestinal manifestations of IL-10 receptor deficiency, especially in the setting of delayed stem cell transplantation.

Convalescent plasma (CP) has been the first line of defense against numerous infectious diseases throughout history. The COVID-19 pandemic created a need for a quick, easily accessible, and effective treatment for severe disease and CP was able to meet that immediate need. The utility of CP warrants a better understanding of the pharmacokinetics of CP treatment. Here we present the case of a COVID-19 patient with a genetic deficiency in antibody production who received CP as a part of the treatment regimen. In depth serological analysis revealed a surprising lack of SARS-CoV-2 specific antibodies and reduced serum IgG following CP infusion. Our study highlights plasma dilution and accelerated antibody clearance as potential mechanisms for the variable efficacy of CP therapy.

From asymptomatic to severe, SARS-CoV-2, causative agent of COVID-19, elicits varying disease severities. Moreover, understanding innate and adaptive immune responses to SARS-CoV-2 is imperative since variants such as Omicron negatively impact adaptive antibody neutralization. Severe COVID-19 is, in part, associated with aberrant activation of complement and Factor XII (FXIIa), initiator of contact system activation. Paradoxically, a protein that inhibits the three known pathways of complement activation and FXIIa, C1 esterase inhibitor (C1-INH), is increased in COVID-19 patient plasma and is associated with disease severity. Here we review the role of C1-INH in the regulation of innate and adaptive immune responses. Additionally, we contextualize regulation of C1-INH and SERPING1, the gene encoding C1-INH, by other pathogens and SARS viruses and propose that viral proteins bind to C1-INH to inhibit its function in severe COVID-19. Finally, we review the current clinical trials and published results of exogenous C1-INH treatment in COVID-19 patients.

Fibromyalgia is characterized by widespread musculoskeletal and joint pain, stiffness, fatigue, and sleep and mood disorders. However, the involvement of the immune system in the pathways of fibromyalgia is unclear. The aim of this study was to explore the role of the immune system in comparison with healthy controls and in association with clinical symptoms. Thirteen women with fibromyalgia and 14 controls were included. Peripheral blood mononuclear cells were stimulated and analysed by flow cytometry, and interferon gamma (IFN-γ) and interleukins were measured. Among clinical symptoms, the fibromyalgia group showed decreased cold pain threshold. Immunologically, they had a higher percentage of monocytes, a lower percentage of CD19⁺ B-cells, and lower secretion of IFN-γ after stimulation. Decreased capacity to secrete IFN-γ was significantly correlated with decreased cold pain threshold in the fibromyalgia group. These results confirm the presence of immune aberrations in fibromyalgia, at least partially responsible for the associated pain.

Infection with SARS-CoV-2 (COVID-19) virus is characterized by an acute respiratory viral illness, often accompanied by extrapulmonary manifestations. Musculoskeletal symptoms such as myalgias and arthralgias are observed in 60 – 70% of cases. Inflammatory arthritis associated with SARS-CoV-2 infection has been reported in the literature, however, nearly all such cases describe a post-viral or reactive phenomenon occurring a few weeks following the infection. We report a unique case of de novo arthritis at the onset of a confirmed COVID-19 infection in a 55-year-old woman. Magnetic resonance imaging demonstrated synovial enhancement consistent with synovitis. Her disease was deemed refractory after failing several immunosuppressive agents. Lastly, we compare our patient's clinical presentation with two other similar cases to understand the natural history of this emerging syndrome.

Since December 2019 the world has been dealing with a severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) pandemic. The first SARS-CoV-2 vaccine was made available in Europe at the end of 2020. 202 volunteers from the vicinity of the University of Applied Sciences Wiener Neustadt took part in this study; their IgG levels recognizing the RBD of SARS-CoV-2 were determined. The aim was to evaluate the SARS-CoV-2 titer levels of vaccinated, recovered and vaccinated plus recovered persons. We could show that there is a significant difference in the antibody levels of vaccinated, vaccinated plus recovered and only recovered probands. Additionally, the highest antibody levels were found in triple vaccinated persons. Furthermore, the Moderna vaccine seems to have a higher immune response.

Introduction

Myocarditis is an adverse reaction discovered after the marketing of SARS-CoV-2 mRNA vaccines. Nevertheless, this effect is not mentioned as an adverse reaction in the summary of product characteristics of other types of vaccines against this disease.

Objective

In this work, we aim to present the cases of myocarditis after vaccination against COVID-19 reported to the national Tunisian centre of pharmacovigilance.

Method

We present the cases of myocarditis reported after the COVID-19 vaccination. All cases are diagnosed according to Brighton's case definition of myocarditis. The vaccines causality assessment was estimated by the French imputability updated method of Bégaud et al.

Results

We included five patients. The sex ratio (M/F) was 4. The mean age was 30 years. All patients had no notable cardiovascular history and did not report any significant past medical history. The onset of symptoms was two days post-vaccination in three patients. The predominant reported symptoms are chest pain and dyspnea in the five cases. Cardiac magnetic resonance imaging (MRI) confirmed the myocarditis diagnosis in four patients (not performed for one patient).

All cases were classified as definitive cases according to the Brighton case definition of myocarditis. No patient required hospitalization in a cardiac intensive care unit. All the patients recovered from acute myocarditis within a few days.

Conclusion

Reported cases of myocarditis post-COVID-19 vaccination in our population are rare, not severe, and have a quick favorable outcome.

Preeclampsia (PE) is a pregnancy-related disorder associated with increasing maternal death rates and affecting 2–8% of pregnant women worldwide. Arterial hypertension and proteinuria, followed by other maternal dysfunctions are classic clinical parameters to identify this disease. Furthermore, hyperuricemia is strictly related to PE, and high plasmatic levels of uric acid have been associated with disease severity. The inflammation in the endothelium caused by danger signals, such as uric acid crystals, is persistent and stimulates the release of inflammatory cytokines, and activates the NLRP3 inflammasome. The mechanisms underlying endothelial dysfunction induced by the metabolism of uric acid, and consequently increased levels of inflammation and oxidative stress in women with PE could be ameliorated with interventions related to inhibition of the NLRP3 activation MSU-mediated and may improve the prognostics of this disease.

Chronic kidney disease (CKD) is one of the major public health problems worldwide, and inflammation is a noticeable cause of CKD. A total of 5508 non-CKD patients were enrolled in our prospective study and followed for three years, with 1.25% (n = 69) participants having newonset CKD at the endpoint. After adjustment for potential confounders, we found that High NLR and low LYMPH% are two independent risk factors for new-onset CKD: Compared with the lowest NLR tertile, the multifactor corrected OR (95% CI) of the highest tertile was 2.47(1.20–5.09), P = 0.014; And adjusted OR (95% CI) was 0.31(0.16–0.62) for the highest LYMPH% tertile, P = 0.001. The model constructed with NLR, LYMPH%, and other risk factors had favourable predictive power for new-onset CKD with an AUC of 0.82 (95% CI, 0.76–0.88). Assessment of NLR and LYMPH% may be helpful for early warning of CKD occurrence.