Activating autoantibodies against G protein-coupled receptors in narcolepsy type 1

Orjatsalo, Maija; Partinen, Eemil; Wallukat, Gerd; Alakuijala, Anniina; Partinen, Markku

doi:10.1016/j.sleep.2020.11.038

Cited by 9 publications

(6 citation statements)

References 45 publications

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“…Their prevalence in the studied group exceeded 90%, indicating that most of the convalescents had their combination. Such a pair of antibodies against beta 2 ‐adrenoceptor and muscarinic receptor was previously reported for patients suffering from dysautonomia, complex regional pain syndrome, narcolepsy type 1, postural orthostatic tachycardia syndrome, and small fiber disease, indicating their broad pathological spectrum 96–98 …”

Section: Autoantibodies Against G Protein‐coupled Receptors (Gpcr)mentioning

confidence: 56%

“…Such a pair of antibodies against beta 2 -adrenoceptor and muscarinic receptor was previously reported for patients suffering from dysautonomia, complex regional pain syndrome, narcolepsy type 1, postural orthostatic tachycardia syndrome, and small fiber disease, indicating their broad pathological spectrum. [96][97][98] Moreover, there are also reports on the presence of autoantibodies against the angiotensin II AT1 receptor (inducing positive chronotropic response on its target) and the angiotensin 1−7 MAS receptor (inducing negative chronotropic effect), both belonging to the renin-angiotensin system and involved in vasoactive processes. 75,95,99 The former ones were previously reported to be involved in severe hypertension and preeclampsia.…”

Section: Autoantibodies Against G Protein-coupled Receptors (Gpcr)mentioning

confidence: 99%

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Overview of autoantibodies in COVID‐19 convalescents

Dobrowolska

Zarębska-Michaluk

Siller‐Matula

et al. 2023

Journal of Medical Virology

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Accumulating evidence shows that SARS‐CoV‐2 can potentially trigger autoimmune processes, which can be responsible for the long‐term consequences of COVID‐19. Therefore, this paper aims to review the autoantibodies reported in COVID‐19 convalescents. Six main groups were distinguished: (i) autoantibodies against components of the immune system, (ii) autoantibodies against components of the cardiovascular system, (iii) thyroid autoantibodies, (iv) autoantibodies specific for rheumatoid diseases, (v) antibodies against G‐protein coupled receptors, and (vi) other autoantibodies. The evidence reviewed here clearly highlights that SARS‐CoV‐2 infection may induce humoral autoimmune responses. However, the available studies share number of limitations, such as: (1) the sole presence of autoantibodies does not necessarily implicate the clinically‐relevant risks, (2) functional investigations were rarely performed and it is often unknown whether observed autoantibodies are pathogenic, (3) the control seroprevalence, in healthy, noninfected individuals was often not reported; thus it is sometimes unknown whether the detected autoantibodies are the result of SARS‐CoV‐2 infection or the accidental post‐COVID‐19 detection, (4) the presence of autoantibodies was rarely correlated with symptoms of the post‐COVID‐19 syndrome, (5) the size of the studied groups were often small, (6) the studies focused predominantly on adult populations, (7) age‐ and sex‐related differences in seroprevalence of autoantibodies were rarely explored, (8) genetic predispositions that may be involved in generation of autoantibodies during SARS‐CoV‐2 infections were not investigated, and (9) the autoimmune reactions following infection with SARS‐CoV‐2 variants that vary in the clinical course of infection remain unexplored. Further longitudinal studies are advocated to assess the link between identified autoantibodies and particular clinical outcomes in COVID‐19 convalescents.

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Section: Autoantibodies Against G Protein‐coupled Receptors (Gpcr)mentioning

confidence: 56%

Section: Autoantibodies Against G Protein-coupled Receptors (Gpcr)mentioning

confidence: 99%

Overview of autoantibodies in COVID‐19 convalescents

Dobrowolska

Zarębska-Michaluk

Siller‐Matula

et al. 2023

Journal of Medical Virology

View full text Add to dashboard Cite

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“…The exact autoimmune processes that cultivate narcolepsy remain to be explained. Initial hypotheses were focused on specific antibodies 29,33–37 ; however, recent findings more strongly support T‐cell‐mediated cellular damage in patients with specific polymorphisms in the alpha locus of the T‐cell receptor 38,39 . The damage inflicted by T‐cells following infections may be triggered via molecular mimicry or as a side effect of systemic hyper‐activation of the immune system and cytokine storms 6,9 .…”

Section: Discussionmentioning

confidence: 99%

“…Initial hypotheses were focused on specific antibodies 29,[33][34][35][36][37] ; however, recent findings more strongly support T-cell-mediated cellular damage in patients with specific polymorphisms in the alpha locus of the T-cell receptor. 38,39 The damage inflicted by T-cells following infections may be triggered via molecular mimicry or as a side effect of systemic hyper-activation of the immune system and cytokine storms. 6,9 Our patient developed typical symptoms of narcolepsy-catalepsy after infection with COVID-19; this concurrence may point to an underlying autoimmune or para-infectious process causing sleep disruption in our patient.…”

Section: Discussionmentioning

confidence: 99%

Narcolepsy following COVID‐19: A case report and review of potential mechanisms

Roya,

Farzaneh,

Mostafa

et al. 2023

Clinical Case Reports

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“…The exact autoimmune processes that cultivate narcolepsy remain to be explained. Initial hypotheses were focused on specific antibodies [27][28][29][30][31][32] ; however, recent findings more strongly support a T-cell-mediated cellular damage in patients with specific polymorphisms in alpha locus of the T-cell receptor 33,34 . The damage inflicted by T-cells following infections may be triggered via molecular mimicry or as a side effect of systemic hyper-activation of the immune system and cytokine storms 4,8 .…”

Section: Discussionmentioning

confidence: 99%