Molecular insights into onset of autoimmunity in SARS‐CoV‐2 infected patients

Laxminarayana, Dama

doi:10.1002/rai2.12056

Cited by 8 publications

(7 citation statements)

References 35 publications

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“…Although they were not enriched in autoreactive B cells, two distinct memory populations (CD80+/ISG15+ and CD11c+/SOX5+/T-bet+/−) with signs of autoreactivity were identified, which were considered to be the source of COVID-19 autoantibodies [ 88 ]. Indeed, the evidence of the development of autoimmune conditions following COVID-19 has accumulated during the past few years [ 44 , 89 , 90 , 91 , 92 , 93 , 94 , 95 ]. In addition, we found a correlation between IL-21 and CVID severity score in patients with CVID.…”

Section: Discussionmentioning

confidence: 99%

Cytokine Response Following SARS-CoV-2 Antigen Stimulation in Patients with Predominantly Antibody Deficiencies

Lucane

Šlisere

Gersone

et al. 2023

Viruses

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Predominantly antibody deficiencies (PADs) are inborn disorders characterized by immune dysregulation and increased susceptibility to infections. Response to vaccination, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may be impaired in these patients, and studies on responsiveness correlates, including cytokine signatures to antigen stimulation, are sparse. In this study, we aimed to describe the spike-specific cytokine response following whole-blood stimulation with SARS-CoV-2 spike peptides in patients with PAD (n = 16 with common variable immunodeficiency and n = 15 with selective IgA deficiency) and its relationship with the occurrence of coronavirus disease 2019 (COVID-19) during up to 10-month follow-up period. Spike-induced antibody and cytokine production was measured using ELISA (anti-spike IgG, IFN-γ) and xMAP technology (interleukin-1β (IL-1β), IL-4, IL-6, IL-10, IL-15, IL-17A, IL-21, TNF-α, TGF-β1). No difference was found in the production of cytokines between patients with PAD and controls. Anti-spike IgG and cytokine levels did not predict contraction of COVID-19. The only cytokine that distinguished between vaccinated and naturally infected unvaccinated PAD patients was IFN-γ (median 0.64 (IQR = 1.08) in vaccinated vs. 0.10 (IQR = 0.28) in unvaccinated). This study describes the spike-specific cytokine response to SARS-CoV-2 antigens, which is not predictive of contracting COVID-19 during the follow-up.

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Section: Discussionmentioning

confidence: 99%

Cytokine Response Following SARS-CoV-2 Antigen Stimulation in Patients with Predominantly Antibody Deficiencies

Lucane

Šlisere

Gersone

et al. 2023

Viruses

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“…During SARS-CoV-2 infections, the host immune system can activate expression of the apolipoprotein B editing catalytic polypeptide 3G and F (APOBEC3G/F) and adenosine deaminase RNA1-specific (ADAR1) genes, which leads to editing the viral RNA and host transcriptome. This response can trigger the production of autoantigens, perceived as foreign by the immune system, and therefore promotes the production of autoantibodies and potentially induces transient or chronic autoimmune diseases [78]. Thus, the viral infection could activate T cells that recognize pancreatic antigens, leading to an autoimmune attack on beta cells and the subsequent development of T1DM.…”

Section: Molecular Mimicrymentioning

confidence: 99%

New-Onset Diabetes Mellitus after COVID-19: Combined Effects of SARS-CoV-2 Variants, Molecular Mimicry, and m6A RNA Methylation

Batista-Roche,

Mirabent-Casals,

Manzanares

et al. 2024

COVID

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Post-COVID syndrome, also known as long COVID, includes a range of symptoms that persist for months or even years after initial infection such as fatigue, shortness of breath, joint pain, chest pain, muscle aches, and heart palpitations, among others. In addition, long COVID is related with new-onset diseases such as diabetes mellitus. The association between SARS-CoV-2 infections and the development of diabetes mellitus is complex and not fully understood. Therefore, the objective of this article was to summarize the state of the art in possible mechanisms involved in the development of diabetes mellitus in the post-COVID-19 era, particularly the impact of SARS-CoV-2 variants on molecular mimicry, the role of viral m6A RNA methylation, and the potential associations between these factors. A better understanding of the combinatorial effects of these mechanisms is paramount for both clinicians and researchers alike because it could help tailor more effective treatment strategies, enhance patient care, and guide future research efforts.

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“…Currently, viruses that have been confirmed to be related to autoimmunity include EBV, CMV, IAV, rotavirus, parvovirus B19 and so on [43]. In addition, since the COVID‐19 pandemic, some infected patients have been clinically observed to develop some confirmed autoimmune diseases or associated autoimmune syndromes secondary to infection, such as RA, SLE and Guillain‐Barrė syndrome [44–47]. These findings provide substantial evidence that viral infections can trigger autoimmunity.…”

Section: The Immunology Of Virus Infectionmentioning

confidence: 99%

New sights of low dose IL‐2: Restoration of immune homeostasis for viral infection

Su,

Zhang,

Wang

et al. 2023

Immunology

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Viral infection poses a significant threat to human health. In addition to the damage caused by viral replication, the immune response it triggers often leads to more serious adverse consequences. After the occurrence of viral infection, in addition to the adverse consequences of infection, chronic infections can also lead to virus‐related autoimmune diseases and tumours. At the same time, the immune response triggered by viral infection is complex, and dysregulated immune response may lead to the occurrence of immune pathology and macrophage activation syndrome. In addition, it may cause secondary immune suppression, especially in patients with compromised immune system, which could lead to the occurrence of secondary infections by other pathogens. This can often result in more severe clinical outcomes. Therefore, regarding the treatment of viral infections, restoring the balance of the immune system is crucial in addition to specific antiviral medications. In recent years, scientists have made an interesting finding that low dose IL‐2 (ld‐IL‐2) could potentially have a crucial function in regulating the immune system and reducing the chances of infection, especially viral infection. Ld‐IL‐2 exerts immune regulatory effects in different types of viral infections by modulating CD4+T subsets, CD8+T cells, natural killer cells, and so on. Our review summarised the role of IL‐2 or IL‐2 complexes in viral infections. Ld‐IL‐2 may be an effective strategy for enhancing host antiviral immunity and preventing infection from becoming chronic; additionally, the appropriate use of it can help prevent excessive inflammatory response after infection. In the long term, it may reduce the occurrence of infection‐related autoimmune diseases and tumours by promoting the restoration of early immune homeostasis. Furthermore, we have also summarised the application of ld‐IL‐2 in the context of autoimmune diseases combined with viral infections; it may be a safe and effective strategy for restoring immune homeostasis without compromising the antiviral immune response. In conclusion, focusing on the role of ld‐IL‐2 in viral infections may provide a new perspective for regulating immune responses following viral infections and improving prognosis.

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Molecular insights into onset of autoimmunity in SARS‐CoV‐2 infected patients

Cited by 8 publications

References 35 publications

Cytokine Response Following SARS-CoV-2 Antigen Stimulation in Patients with Predominantly Antibody Deficiencies

Cytokine Response Following SARS-CoV-2 Antigen Stimulation in Patients with Predominantly Antibody Deficiencies

New-Onset Diabetes Mellitus after COVID-19: Combined Effects of SARS-CoV-2 Variants, Molecular Mimicry, and m6A RNA Methylation

New sights of low dose IL‐2: Restoration of immune homeostasis for viral infection

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