Welcome to the Autoimmunity 2021 Congress Calendar
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THE SARS-CoV-2 AS AN INSTRUMENTAL TRIGGER OF AUTOIMMUNITY
COVID - 19 AND AUTOIMMUNITY
INFLAMMATION IN COVID-19
Past COVID-19 patients: Vaccine yes or vaccine NOT?
EFFECTIVENESS OF INTERLEUKIN-1 AND INTERLEUKIN-6 INHIBITION COMPARED TO STANDARD MANAGEMENT IN PATIENTS WITH COVID-19 AND HYPERINFLAMMATION: A COHORT STUDY
Abstract
Background and Aims
Patients with severe COVID-19 develop a life-threatening hyper-inflammatory response to the virus. Treatment with interleukin (IL)-1 or IL-6 inhibitors has been used to treat this patient population, but the comparative effectiveness of these different strategies remains undetermined.
Methods
Retrospective cohort study of in-hospital patients with COVID-19, respiratory insufficiency, and hyperinflammation, defined as serum C-reactive protein (CRP) ≥100 mg/L and/or ferritin ≥900 ng/ml. The primary endpoint was survival; secondary endpoint was a composite of death or mechanical ventilation. Multivariable Cox regression analysis and interaction tests were conducted.
Results
Of 392 included patients, 275 did not receive IL inhibitors, 62 received the IL-1 inhibitor anakinra, and 55 received an IL-6 inhibitor (tocilizumab, n=29; sarilumab, n=26). At multivariable analysis, patients treated with IL-1 inhibition, but not with IL-6 inhibition, had a significantly reduced mortality risk compared to patients who did not receive IL inhibitors (Hazard Ratios 0.45; 95% CI 0.20-0.99, p=0.04, and 0.90; 95% CI 0.41-1.97; p=0.8, respectively). At interaction tests IL-6 inhibition was effective in a subgroup of patients with markedly high CRP levels, whereas both IL-1 and IL-6 inhibition were more effective in patients with low LDH levels.
Conclusions
IL-1 inhibition, but not IL-6 inhibition, was associated with a significant reduction of mortality in hospitalized patients with COVID-19 and hyperinflammation. IL-6 inhibition was effective in a subgroup of patients with markedly high CRP levels, whereas both IL-1 and IL-6 inhibition were more effective in patients with low LDH levels.
NATURAL KILLER (NK) CELL DYSFUNCTION, COVID-19 AND IMMUNE DYSREGULATION
Abstract
Background and Aims
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections resulting in coronavirus disease 2019 (COVID-19) is characterized by a clinical constellation consisting of pro-inflammatory cytokine release, organ damage and/or death. Imbalanced immunoregulatory mechanisms during viral infection are potential drivers of this. In this study, we pursued the hypothesis that NK cell dysfunction is a prominent feature of COVID-19 that is associated with a decreased abundance of cytokines required for NK cell functions (e.g. interleukin (IL)15, 12 and 21).
Methods
Only patients with severe COVID-19 were enrolled in our study. Peripheral blood collected within 24-48H of COVID-19 confirmation was used to enumerate NK cells (CD45+CD3-CD56+CD16+/-), CD56bright/dim subsets, and NK-cell functional activities (surface CD107a (degranulation) and intracellular interferon-γ (IFN-γ)) via flow cytometry. Luminex immunoassays were used to determine the serum concentrations of IL12, IL15 and IL21, and soluble CD25 (sCD25)/soluble IL2 receptor α (sIL2-Rα) (R&D Systems Inc). Results from COVID-19 patients were compared with those obtained from healthy controls using Mann-Whitney U statistics. Where applicable, correlation analyses were performed using Spearman rank correlation.
Results
Significantly impaired NK-cell counts and cytolytic activity were observed in COVID-19 patients compared with healthy controls. Also, IL12, IL15, and IL18 were not detected systematically. Serum concentrations of sCD25 were significantly elevated and were inversely correlated with the percentage of NK cells.
Conclusions
Impaired NK-cell cytolytic activity together with elevated sCD25 were consistent with our hypothesis. Together, these findings suggest that impaired counts and cytolytic NK cell activity are important characteristics of severe COVID-19 which can be potentially utilized in future immunomodulatory approaches.
SARS-COV2: AUTOIMMUNITY AND CLINICAL OUTCOMES.
Abstract
Background and Aims
In December 2019 a novel outbreak of a new strain of coronavirus infection emerged. The SARS-CoV-2 or the Covid-19 was declared as a pandemic and is characterized by fever, dry cough, myalgia and or extreme fatigue. Some patients are asymptomatic, but in a few cases it may present as a disease characterized by immune hyperactivation, which increases the severity and mortality in these patients. It has been suggested that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and / or autoinflammatory dysregulation. Our aim is to correlate the development of autoimmunity with the severity of the desease
Methods
Our patient cohort was obtained from hospital records, selecting only those patients admitted to hospital where inflammatory markers and autoimmunity tests were studied.
Results
We studied a total of 60 patients, in whom we analyzed and correlated the following variables: age, sex, CRP, ferritin, d-dimer, LDH, IL6, use of tocilizumab, ICU admission and days of hospitalization.
Conclusions
The association between autoimmunity and viral infections has been previously described, but the hypothesis that this phenomenon may modify the clinical course requires particular attention. So far, studies correlating the occurrence of autoimmunity and the clinical outcome in the short and long-term are scarce. Further studies are needed to explore the importance of this phenomenon in this new scenario.
CORONAVIRUS-ASSOCIATED MOLECULAR MIMICRY THROUGH HOMOLOGY TO A 15MER SARS-COV-2 PEPTIDE
Abstract
Background and Aims
COVID-19 pathogenicity can be involving autoimmunity. In relation, the aim in this study is to look for autoimmunity-related pathological mechanisms common to certain coronaviruses, including SARS-CoV-2, through a 15mer (CFLGYFCTCYFGLFC), which is part of the SARS-CoV-2 nsp6 protein.
Methods
Coronavirus-associated sequences, which are homologous to the specific SARS-CoV-2 peptide, are obtained. Then we found the alignments of those homologous coronavirus sequences with the human sequences, with at least 7 residue matches, and also common to the selected SARS-CoV-2 15mer peptide alignments with the human sequences. Finally, epitope pairs that are sourced by those coronavirus and human sequences are identified. However, for that, the epitope pairs were expected to be predicted to bind strongly to the same HLA alleles while those HLA alleles are the same also as that of the epitope pairs, which are sourced by the respective alignments of the SARS-CoV-2 15mer.
Results
Proteins or protein regions that contain those predicted epitopes are immunoglobulin heavy chain junction regions, CRB1 isoform I precursor, slit homolog 2 protein, hCG1995581, hCG2028737, and phospholipid phosphatase-related protein type 2. They are possibly correlated with certain pathological conditions. Among those, CRB1 isoform I precursor is aligning with the highest number of different coronavirus sequences, which are homologous to the SARS-CoV-2 peptide, and its relevant query-subject epitope pairs have strong binding affinity to the HLA-A*24:02 allele.
Conclusions
Results imply autoimmunity risk in COVID-19 patients with HLA-A*02:01 and HLA-A*24:02 serotypes, through molecular mimicry, which is common to those sourced by other coronaviruses than SARS-CoV-2, and to SARS-CoV-2, at different extents.