Back to Search
Start Over
Anti-AT1R autoantibodies and prediction of the severity of Covid-19
- Source :
- Human Immunology
- Publication Year :
- 2022
- Publisher :
- Elsevier BV, 2022.
-
Abstract
- The stimulation of AT1R (Angiotensin II Receptor Type 1) by Angiotensin II has, in addition to the effects on the renin-angiotensin system, also pro-inflammatory effects through stimulation of ADAM17 and subsequent production of INF-gamma and Interleukin-6. This pro-inflammatory action stimulate the cytokine storm that characterizes the most severe forms of SARS-CoV-2 infection. We studied the effect of AT1Rab on the AT1R on 74 subjects with SARS-CoV-2 infection with respiratory symptoms requiring hospitalization. We divided the patients into 2 groups: 34 with moderate and 40 with severe symptoms that required ICU admission. Hospitalized subjects showed a 50% reduction in the frequency of AT1Rab compared to healthy reference population. Of the ICU patients, 33/40 (82.5%) were AT1Rab negative and 16/33 of them (48.5%) died. All 7 patients positive for AT1Rab survived. These preliminary data seem to indicate a protective role played by AT1R autoantibodies on inflammatory activation in SARS-CoV-2 infection pathology.
- Subjects :
- Adult
Male
Angiotensin II
AT1R autoantibodies
SARS-CoV-2 infection
medicine.medical_specialty
Coronavirus disease 2019 (COVID-19)
Short Communication
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Immunology
Stimulation
Autoantigens
SARS-CoV-2, severe acute respiratory syndrome coronavirus 2
Gastroenterology
Receptor, Angiotensin, Type 1
Internal medicine
medicine
Humans
Immunology and Allergy
Respiratory system
AngII, Angiotensin II
Aged
Autoantibodies
Retrospective Studies
Aged, 80 and over
Angiotensin II receptor type 1
SARS-CoV-2
business.industry
Autoantibody
COVID-19
General Medicine
Middle Aged
medicine.disease
ACE-2, Angiotensin Converting Enzyme
Hospitalization
Italy
Female
business
Cytokine storm
AT1Rab, autoantibodies direct vs Angiotensin II Receptor1
Subjects
Details
- ISSN :
- 01988859
- Volume :
- 83
- Database :
- OpenAIRE
- Journal :
- Human Immunology
- Accession number :
- edsair.doi.dedup.....072859fa313f38d2ce140b2f398e7d77