Autoimmune diseases occur when the immune system becomes hyperactive and fails to recognize the body's own organs and tissues. This leads to inflammation, tissue damage, and long-term complications. Examples include rheumatoid arthritis, multiple sclerosis, psoriasis, vitiligo, lupus erythematosus, immune-mediated glomerulopathies, dermatoses, scleroderma, and graft-versus-host disease.
The core issue in these conditions is immune system over activation, which can be triggered by epigenetic changes, environmental factors, or external agents.
Regulatory T cells (Tregs) play a vital role in modulating immune responses. They help control the activation of cytotoxic T lymphocytes—particularly CD4 and CD8 cells—to prevent them from attacking the body's own tissues.
In individuals with autoimmune diseases, this regulatory mechanism is impaired. Traditional treatments aim to reduce the overall number of lymphocytes to manage inflammation, but unfortunately, these drugs are non-selective and also deplete Tregs—worsening immune imbalance.
Image reference: Comparison of healthy vs. arthritic joint showing immune cell activity
Treg-based therapies aim to increase the number and activity of regulatory T cells to restore immune balance and reduce disease activity.
In addition, monoclonal antibody therapies such as Rituximab have shown effectiveness in decreasing chronic inflammation and supporting immune system function.
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