HOW TO PREVENT DEVELOPMENT OF SEVERE COVID-19 DISEASE
Evidence suggests that targeting innate lymphoid cells (ILCs) may be beneficial in the design of therapeutics for COVID-19 generated autoimmune disorders. As ILCs and T cells have many redundant functions, targeting and neutralizing their effector cytokines might be a better option. Alternatively, targeting their upstream activating mediators (IL-23, IL-1B, or IL-6), or their survival factors (IL-7) could be used as an approach to treat inflammatory diseases.
The epithelium comprises a physical barrier, which together with the mucus layer and production of anti-microbial peptides provides a containment barrier, which confines microbes in the lumen. The innate lymphoid cells residing in the immune compartment of the lamina propria, which is a thin layer of connective tissue that forms part of the moist linings known as mucous membranes or mucosa, which line various tubes in the body, such as the respiratory tract, the gastrointestinal tract, and the urogenital tract, are key early warning sentinels detecting invading pathogens through conserved pattern recognition receptors, such as toll-like receptors. Pathogen detecting populations, include cells of the mononuclear phagocyte system, including macrophages and dendritic cells (DCs), which engulf and process microbial antigens and present the antigens to adaptive immune cells, thus providing initial signals to adaptive immune system lymphocytes to engage potent antigen-specific T and B cell responses.
Innate lymphoid cells (ILCs) are distributed throughout the human body in lymphoid and non-lymphoid tissues, but are especially enriched at the mucosal barrier surfaces, where they directly interact with a number of different cell types; hematopoietic or other . ILCs have lymphoid-like morphology, but lack any antigen-specific receptors. Arising from a common lymphoid progenitor and similarly to T cells, they can be further subdivided into phenotypically and functionally distinct populations that produce different combinations of effector cytokines to mediate their functions. Their development depends on different transcription factors, which are also used to help divide ILCs into 5 main groups; group 1 ILCs that includes Natural Killer cells, as well as the non-cytotoxic ILC1s, group 2 ILCs or ILC2s, group 3 ILCs including ILC3s, group 4 containing lymphoid tissue inducer (LTi) cells and, group 5 are regulatory ILCs or ILCregs.
The production of Interleukin-5 (IL-5) by ILC2s in the lung leads to eosinophil recruitment, and other cell populations interact and shape the presence of lung ILC2s in airway inflammation. In addition, they also promote proliferation of B cells. It seems, that the increase in ILC2s present correlates with the severity of inflammation in the lungs, intestines, kidneys and other organs of patients suffering from severe COVID-19, and evidence confirms some ‘immunogen- experienced’ ILC2s persist after the resolution of the initial inflammation, portraying similarities to memory T cells. So, people who have been previously exposed to other coronaviruses may carry some some "Immunogen-experienced" ILC2s in the in the immune compartment of their lamina propria, that can provide at least partial protection against SARS-CoV-2.
It has been shown in mice that Natural Killer cells (NK cells) and ILC1s inhibit ILC2 expansion due to the production of Interferon- Gamma, and therefore they (NK cells and non- cytotoxic group 1 Innate Lymphocyte Cells) may help prevent the development of severe COVID-19 disease.
I intend to support my thesis, that the primary obligatory weapon against SARS-COV-2 is our highly complex and ancient, innate immune system, and not the simple, modern adaptive immune system.
Universe is a zero dimensional infinity.
Evidence suggests that targeting innate lymphoid cells (ILCs) may be beneficial in the design of therapeutics for COVID-19 generated autoimmune disorders. As ILCs and T cells have many redundant functions, targeting and neutralizing their effector cytokines might be a better option. Alternatively, targeting their upstream activating mediators (IL-23, IL-1B, or IL-6), or their survival factors (IL-7) could be used as an approach to treat inflammatory diseases.
The epithelium comprises a physical barrier, which together with the mucus layer and production of anti-microbial peptides provides a containment barrier, which confines microbes in the lumen. The innate lymphoid cells residing in the immune compartment of the lamina propria, which is a thin layer of connective tissue that forms part of the moist linings known as mucous membranes or mucosa, which line various tubes in the body, such as the respiratory tract, the gastrointestinal tract, and the urogenital tract, are key early warning sentinels detecting invading pathogens through conserved pattern recognition receptors, such as toll-like receptors. Pathogen detecting populations, include cells of the mononuclear phagocyte system, including macrophages and dendritic cells (DCs), which engulf and process microbial antigens and present the antigens to adaptive immune cells, thus providing initial signals to adaptive immune system lymphocytes to engage potent antigen-specific T and B cell responses.
Innate lymphoid cells (ILCs) are distributed throughout the human body in lymphoid and non-lymphoid tissues, but are especially enriched at the mucosal barrier surfaces, where they directly interact with a number of different cell types; hematopoietic or other . ILCs have lymphoid-like morphology, but lack any antigen-specific receptors. Arising from a common lymphoid progenitor and similarly to T cells, they can be further subdivided into phenotypically and functionally distinct populations that produce different combinations of effector cytokines to mediate their functions. Their development depends on different transcription factors, which are also used to help divide ILCs into 5 main groups; group 1 ILCs that includes Natural Killer cells, as well as the non-cytotoxic ILC1s, group 2 ILCs or ILC2s, group 3 ILCs including ILC3s, group 4 containing lymphoid tissue inducer (LTi) cells and, group 5 are regulatory ILCs or ILCregs.
The production of Interleukin-5 (IL-5) by ILC2s in the lung leads to eosinophil recruitment, and other cell populations interact and shape the presence of lung ILC2s in airway inflammation. In addition, they also promote proliferation of B cells. It seems, that the increase in ILC2s present correlates with the severity of inflammation in the lungs, intestines, kidneys and other organs of patients suffering from severe COVID-19, and evidence confirms some ‘immunogen- experienced’ ILC2s persist after the resolution of the initial inflammation, portraying similarities to memory T cells. So, people who have been previously exposed to other coronaviruses may carry some some "Immunogen-experienced" ILC2s in the in the immune compartment of their lamina propria, that can provide at least partial protection against SARS-CoV-2.
It has been shown in mice that Natural Killer cells (NK cells) and ILC1s inhibit ILC2 expansion due to the production of Interferon- Gamma, and therefore they (NK cells and non- cytotoxic group 1 Innate Lymphocyte Cells) may help prevent the development of severe COVID-19 disease.
I intend to support my thesis, that the primary obligatory weapon against SARS-COV-2 is our highly complex and ancient, innate immune system, and not the simple, modern adaptive immune system.
Universe is a zero dimensional infinity.