Autoantibodies against type I IFNs in patients with life-threatening COVID-19

@article{Bastard2020AutoantibodiesAT,
  title={Autoantibodies against type I IFNs in patients with life-threatening COVID-19},
  author={Paul Bastard and Lindsey B. Rosen and Qian Zhang and Eleftherios Michailidis and Hans-Heinrich Hoffmann and Yu Zhang and Karim Dorgham and Quentin Philippot and J{\'e}r{\'e}mie Rosain and Vivien B{\'e}ziat and J{\'e}r{\'e}my Manry and Elana Shaw and Liis Haljasm{\"a}gi and P{\"a}rt Peterson and Lazaro Lorenzo and Lucy Bizien and Sophie Trouillet-Assant and Kerry Dobbs and Adriana Almeida de Jesus and Alexandre Belot and Anne Kallaste and {\'E}milie Catherinot and Yacine Tandjaoui-Lambiotte and J{\'e}r{\'e}mie Le Pen and Gaspard Kerner and Benedetta Bigio and Yoann Seeleuthner and Rui Yang and Alexandre Bolze and Andr{\'a}s N. Spaan and Ottavia Maria Delmonte and Michael S Abers and Alessandro Aiuti and Giorgio Casari and Vito Lampasona and Lorenzo Piemonti and Fabio Ciceri and Kaya Bilguvar and Richard P Lifton and Marc Vasse and David M. Smadja and M{\'e}lanie Migaud and J{\'e}r{\^o}me Hadjadj and Benjamin Terrier and Darragh Duffy and Llu{\'i}s Quintana-Murci and Diederik van de Beek and Lucie Roussel and Donald Cuong Vinh and Stuart G. Tangye and Filomeen Haerynck and David Dalmau and Javier Martinez-Picado and Petter Brodin and Michel C. Nussenzweig and St{\'e}phanie Boisson-Dupuis and Carlos Rodr{\'i}guez-Gallego and Guillaume Vogt and Trine Hyrup Mogensen and Andrew J. Oler and Jingwen Gu and Peter D. Burbelo and Jeffrey I. Cohen and Andrea Biondi and Laura Rachele Bettini and Mariella D'angi{\`o} and Paolo Bonfanti and Patrick Rossignol and Julien Mayaux and Fr{\'e}d{\'e}ric Rieux-Laucat and Eystein Sverre Husebye and Francesca R. Fusco and Matilde Valeria Ursini and Luisa Imberti and Alessandra Sottini and Simone Paghera and Eugenia Quiros-Roldan and Camillo Rossi and Riccardo Castagnoli and Daniela Montagna and Amelia Licari and Gian Luigi Marseglia and Xavier Duval and Jade Ghosn and John S. Tsang and Raphaela Goldbach-Mansky and Kai Kisand and Michail S. Lionakis and Anne Puel and Shen-Ying Zhang and Steven M. Holland and Guy Gorochov and Emmanuelle Jouanguy and Charles M. Rice and Aur{\'e}lie Cobat and Luigi Daniele Notarangelo and Laurent Abel and Helen C. Su and Jean Laurent Casanova},
  journal={Science (New York, N.y.)},
  year={2020},
  volume={370}
}
The genetics underlying severe COVID-19 The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induced inflammation. Two studies now examine the likelihood that genetics affects the risk of severe coronavirus disease 2019 (COVID-19) through components of this… Expand
Inborn errors of type I IFN immunity in patients with life-threatening COVID-19
TLDR
The COVID Human Genetic Effort established to test the general hypothesis that life-threatening COVID-19 in some or most patients may be caused by monogenic inborn errors of immunity to SARS-CoV-2 with incomplete or complete penetrance finds an enrichment in variants predicted to be loss-of-function (pLOF), with a minor allele frequency <0.001. Expand
Dysregulated Interferon Response Underlying Severe COVID-19
TLDR
Current studies call for a better understanding of the IFN response regarding the spatiotemporal determination and subtype-specificity against SARS-CoV-2 infections, which are warranted to devise IFN-related prophylactics and therapies. Expand
Insufficient type I IFN immunity underlies life-threatening COVID-19 pneumonia.
TLDR
Findings indicate that impaired type I IFN immunity underlies life-threatening COVID-19 pneumonia in at least 13% of patients, and pave the way for further research into unexplained severe cases, and provide a rationale for preventing and treating the disease in individuals at risk, with recombinanttype I IFNs. Expand
Autoantibodies against type I interferons are associated with multi-organ failure in COVID-19 patients
TLDR
It is shown that auto-Abs against IFN-I that are not neutralizing in vitro occur frequently in ICU patients (16%), irrespective of COVID-19 infection. Expand
Type I interferon autoantibodies are associated with systemic immune alterations in patients with COVID-19
TLDR
It is suggested that early evidence of type I IFN autoantibodies and increased LAIR1 expression may help distinguish severe cases of COVID-19, the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Expand
Editorial: Autoantibodies to Components of the Immune System, Including Type 1 Interferons, and the Risk of Severe COVID-19
  • D. Parums
  • Medicine
  • Medical science monitor : international medical journal of experimental and clinical research
  • 2021
TLDR
This Editorial aims to present some recent findings of autoantibodies to components of the immune system, including type 1 IFNs, and the risk of severe COVID-19. Expand
Circulating Type I Interferon Levels and COVID-19 Severity: A Systematic Review and Meta-Analysis
TLDR
Peripheral IFN-α cannot be used as a severity marker as it does not determine the clinical status presented by COVID-19 patients. Expand
The Abstruse Side of Type I Interferon Immunotherapy for COVID-19 Cases with Comorbidities
TLDR
The role of IFN-I signaling in infectious and non-infectious diseases of humans is summarized and the precautionary measures to be considered are highlighted before administering IFn-I to COVID-19 patients having other co-existing disorders. Expand
Potential Implications of a Type 1 Interferon Gene Signature on COVID-19 Severity and Chronic Inflammation in Sickle Cell Disease
TLDR
Type 1 interferon responses in patients with SCD may contribute to the variable COVID-19 responses reported in prior studies, and additional studies investigating the mechanisms underlying IFNα/β production and other clinical consequences of IFNβ-mediated inflammation in SCD disease are warranted. Expand
Diverse Functional Autoantibodies in Patients with COVID-19
TLDR
It is established that these autoantibodies perturb immune function and impair virological control by inhibiting immunoreceptor signaling and by altering peripheral immune cell composition, and found that murine surrogates of these autoantsibodies exacerbate disease severity in a mouse model of SARS-CoV-2 infection. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 121 REFERENCES
Inborn errors of type I IFN immunity in patients with life-threatening COVID-19
TLDR
The COVID Human Genetic Effort established to test the general hypothesis that life-threatening COVID-19 in some or most patients may be caused by monogenic inborn errors of immunity to SARS-CoV-2 with incomplete or complete penetrance finds an enrichment in variants predicted to be loss-of-function (pLOF), with a minor allele frequency <0.001. Expand
Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients
TLDR
The results of this trio of studies suggest that the location, timing, and duration of IFN exposure are critical parameters underlying the success or failure of therapeutics for viral respiratory infections. Expand
Development of a Validated Interferon Score Using NanoString Technology.
TLDR
A 28-IFN response gene scoring system is developed to calculate either a standardized or geomean score by customizing a NanoString assay to quantify the expression of putative IRGs and showed high reproducibility and low intra- and interassay variability. Expand
Broad-spectrum antibodies against self-antigens and cytokines in RAG deficiency.
TLDR
It is demonstrated that patients with hypomorphic RAG mutations, especially those with delayed-onset combined immune deficiency and granulomatous/autoimmune manifestations (CID-G/AI), produce a broad spectrum of autoantibodies and indicates that environmental triggers may modulate the phenotypic expression of autoimmune manifestations. Expand
Anti-Interferon Autoantibodies in Autoimmune Polyendocrinopathy Syndrome Type 1
TLDR
These apparently spontaneous autoantibody responses to IFNs, particularly IFN-α and IFn-ω, segregate like a recessive trait; their high “penetrance” is especially remarkable for such a variable condition. Expand
Naturally occurring anti-IFN-gamma autoantibody and severe infections with Mycobacterium cheloneae and Burkholderia cocovenenans.
TLDR
Screening for neutralizing anti-IFN-Gamma autoantibodies should supplement testing for IFN-gamma and IL-12 pathway defects in patients with recurrent infections with intracellular pathogens, especially with nontuberculous mycobacteria. Expand
Acquired predisposition to mycobacterial disease due to autoantibodies to IFN-gamma.
TLDR
It is postulated that acquired defects in macrophage activation by IFN-gamma may cause a similar immunological phenotype and thus explain the occurrence of disseminated intracellular infections in some patients without identifiable immune deficiency. Expand
AIRE-Deficient Patients Harbor Unique High-Affinity Disease-Ameliorating Autoantibodies
TLDR
It is shown that most APS1/APECED patients displayed B cell autoreactivity toward unique sets of approximately 100 self-proteins, and naturally occurring human autoantibodies may actively limit disease and be of therapeutic utility. Expand
Wherefore interferon?
  • I. Gresser
  • Medicine
  • Journal of leukocyte biology
  • 1997
TLDR
Arguments will be presented to support the hypothesis that the major role of IFN is, after all, in antiviral defense, and the use of type I IFN in the treatment of patients with viral and neoplastic diseases and even diseases of varied and unknown etiology is discussed. Expand
Convergent Antibody Responses to SARS-CoV-2 in Convalescent Individuals
TLDR
Most convalescent plasma samples obtained from individuals who recover from COVID-19 do not contain high levels of neutralizing activity, and rare but recurring RBD-specific antibodies with potent antiviral activity were found in all individuals tested, suggesting that a vaccine designed to elicit such antibodies could be broadly effective. Expand
...
1
2
3
4
5
...