Rubio-Casillas, A.; Redwan, E.M.; Uversky, V.N. Does SARS-CoV-2 Induce IgG4 Synthesis to Evade the Immune System? Biomolecules2023, 13, 1338.
Rubio-Casillas, A.; Redwan, E.M.; Uversky, V.N. Does SARS-CoV-2 Induce IgG4 Synthesis to Evade the Immune System? Biomolecules 2023, 13, 1338.
Rubio-Casillas, A.; Redwan, E.M.; Uversky, V.N. Does SARS-CoV-2 Induce IgG4 Synthesis to Evade the Immune System? Biomolecules2023, 13, 1338.
Rubio-Casillas, A.; Redwan, E.M.; Uversky, V.N. Does SARS-CoV-2 Induce IgG4 Synthesis to Evade the Immune System? Biomolecules 2023, 13, 1338.
Abstract
SARS-CoV-2, the virus that causes theCOVID-19 disease, has been demonstrated to cause immune suppression in certain individuals. This can manifest as a reduced ability for the host's immune system to effectively control the infection. Studies have reported that patients with COVID-19 can exhibit a decline in white blood cell counts, including natural killer cells and T cells, which are integral components of the immune system's response to viral pathogens. These cells play critical roles in the immune response to viral infections, and their depletion can make it harder for the body to mount an effective defense against the virus. Additionally, the virus can also directly infect immune cells, further compromising their ability to function. Some individuals with severe COVID-19 pneumonia may develop a "cytokine storm," an overactive immune response that may result in tissue damage and organ malfunction. The underlying mechanisms of immune suppression in SARS-CoV-2 are not entirely comprehended at this time, and ongoing research is being conducted to gain a more comprehensive understanding. Research has shown that severe SARS-CoV-2 infection promotes the synthesis of IgG4 antibodies. In this work, we propose the hypothesis that the IgG4 antibody produced by B cells in response to infection by SARS-CoV2 generates immunological tolerance that prevents its elimination, and leads to persistence and chronic infection. In sum, we believe that this constitutes another immune evasion mechanism that bears striking similarities to that developed by cancer cells to evade immune surveillance.
Keywords
SARS-CoV-2; IgG4; Tregs; long COVID; immune tolerance
Subject
Biology and Life Sciences, Immunology and Microbiology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received:
17 August 2023
The commenter has declared there is no conflict of interests.
Comment:
Thank you.
I can add to this by discussion of the receptors that the virus/spike protein uses to bind to and infect CD4+ T helper lymphocytes, contributing further to ongoing immune suppression:
Received:
17 August 2023
The commenter has declared there is no conflict of interests.
Comment:
A related study of interest regarding anti interferon gamma autoantibodies & igG4.
We find (initially) non-cancerous tumour-like neoplasms with igG4 related disease:
Lymphadenopathy Associated With Neutralizing Anti-interferon-gamma Autoantibodies Could Have Monoclonal T-cell Proliferation Indistinguishable From Malignant Lymphoma and Treatable by Antibiotics: A Clinicopathologic Study (2021) https://pubmed.ncbi.nlm.nih.gov/34010155/
The commenter has declared there is no conflict of interests.
I can add to this by discussion of the receptors that the virus/spike protein uses to bind to and infect CD4+ T helper lymphocytes, contributing further to ongoing immune suppression:
Megathread #33: SARS-CoV-2 infectivity of CD4+ & CD26+/DPP4 T-lymphocyte cells, Tat-like motifs, CCR5, integrin binding and related pathologies
https://doorlesscarp953.substack.com/publish/posts/detail/135861704?referrer=%2Fpublish%2Fhome
Your paper underscores the challenge of developing anti-cancer "vaccines" too.
The commenter has declared there is no conflict of interests.
We find (initially) non-cancerous tumour-like neoplasms with igG4 related disease:
Lymphadenopathy Associated With Neutralizing Anti-interferon-gamma Autoantibodies Could Have Monoclonal T-cell Proliferation Indistinguishable From Malignant Lymphoma and Treatable by Antibiotics: A Clinicopathologic Study (2021)
https://pubmed.ncbi.nlm.nih.gov/34010155/