SARS-CoV-2 Induced IgG Autoantibodies Are Targeting Various Immune Cells and Also Proteins in Various Organs
Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 14, 2025 8 hours, 8 minutes ago
Medical News:
A New Perspective on COVID-19 and Autoimmune Reactions
Researchers from the University of São Paulo, Brazil, have unveiled significant findings on how SARS-CoV-2-induced IgG autoantibodies may be targeting various immune cells and proteins in different tissues and organs. The study sheds light on the potential role of these antibodies in driving autoimmune responses in COVID-19 patients, which could explain some of the persistent complications seen in long COVID and severe cases of the disease.
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ARS-CoV-2 Induced IgG Autoantibodies Are Targeting Various Immune Cells and Also Proteins in Various Organs
The connection between COVID-19 and autoimmune diseases has been a growing area of research. While it has long been suspected that SARS-CoV-2 can trigger autoimmune reactions, this study provides a deeper understanding of the specific targets of these autoantibodies. Using an advanced proteomic approach, scientists analyzed how these antibodies interact with human proteins and assessed their impact on immune functions and various organs.
Study Methodology and Key Findings
To explore the proteomic targets of SARS-CoV-2-induced IgG antibodies, the research team utilized a human proteome microarray consisting of 23,736 unique proteins, including isoforms and protein fragments cataloged in the Human Protein Atlas. Serum samples were collected from four distinct groups: healthy individuals (N-exp HC), vaccinated individuals who received protein-based vaccines (N-Cov Vac), and patients with moderate or severe COVID-19 (COVID-Mod and COVID-Sev).
This
Medical News report highlights that the study findings indicate SARS-CoV-2 infection leads to the production of IgG autoantibodies that can mistakenly target a variety of human proteins. Among the most notable targets identified were:
-Cytokines and growth factors: Interferon-alpha (IFN-α), tumor growth factor-beta (TGF-β), interleukin-1 (IL-1), and CXCL16.
-Cell surface proteins and receptors: TGF-β receptors, CD34, CD47, and BCL2.
Immune cells impacted: CD4+ and CD8+ T cells, γδ T cells, B cells, dendritic cells, and natural killer (NK) cells.
-Proteins in major organs: The autoantibodies also exhibited reactivity toward proteins found in the brain, liver, lungs, and heart.
A crucial aspect of the study was the evaluation of how autoantibody targeting differed based on disease severity. The findings suggest that individuals with severe COVID-19 (COVID-Sev) showed a higher degree of immune protein targeting than those with moderate cases (COVID-Mod). This correlation suggests that disease severity may be directly linked to the extent of autoimmune-like activity in the body.
Implications for Autoimmunity and Long COVID
A fascinating discovery was that individu
als who were vaccinated with protein-based vaccines had IgG autoantibody profiles that closely resembled those of healthy, non-exposed individuals. This suggests that the generation of these potentially harmful autoantibodies is directly associated with active SARS-CoV-2 infection rather than vaccination.
Furthermore, an analysis of the protein-protein interaction network (PPIN) for the targeted proteins revealed that there was minimal structural homology and co-expression among them. This suggests that the autoantibody response is not simply due to cross-reactivity with homologous proteins but could represent a more complex immune reaction that needs further exploration.
What Do These Findings Mean?
The study's findings emphasize that SARS-CoV-2 infection can provoke widespread autoimmune-like responses, potentially contributing to severe COVID-19 outcomes and the lingering symptoms seen in long COVID patients. The identification of IgG autoantibodies targeting critical immune regulatory proteins, cell surface receptors, and organ-specific proteins indicates a need for further research into whether these responses contribute to tissue damage, inflammation, and chronic health issues post-COVID-19.
Given these revelations, scientists now face pressing questions: Are these autoantibodies a transient effect of the infection, or do they persist long after recovery? Could they be responsible for some of the autoimmune diseases reported following COVID-19? And most importantly, could future treatments focus on neutralizing these autoantibodies to mitigate severe COVID-19 and long COVID symptoms?
As the scientific community continues to investigate, this study provides a compelling case for further examining the autoimmune dimension of COVID-19. Understanding how these antibodies function may pave the way for more targeted treatments that can prevent or alleviate the long-term complications of the disease.
The study findings were published in the peer-reviewed journal: Immunology.
https://onlinelibrary.wiley.com/doi/10.1111/imm.13919
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