Infectious tolerance

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Concept in immunology


Infectious tolerance is a phenomenon in immunology where a state of immune tolerance is transferred from one population of immune cells to another. This process is primarily mediated by regulatory T cells (Tregs), which play a crucial role in maintaining immune homeostasis and preventing autoimmunity.

Mechanism[edit | edit source]

Immunoregulation by regulatory T cells (Treg)

Infectious tolerance occurs when Tregs convert other immune cells, such as effector T cells, into additional Tregs or other types of regulatory cells. This conversion is facilitated by the secretion of immunosuppressive cytokines such as interleukin-10 (IL-10) and transforming growth factor beta (TGF-β). These cytokines create an immunosuppressive environment that promotes the development of tolerance in surrounding immune cells.

The process begins when Tregs recognize specific antigens presented by antigen-presenting cells (APCs). Upon recognition, Tregs can suppress the activation and proliferation of effector T cells that are specific to the same antigen. This suppression is not limited to direct cell-to-cell contact but can also affect nearby immune cells, leading to a broader state of tolerance.

Role in Autoimmunity[edit | edit source]

Infectious tolerance is a critical mechanism in preventing autoimmune diseases, where the immune system mistakenly attacks the body's own tissues. By promoting tolerance, Tregs help to prevent the activation of autoreactive T cells that could lead to tissue damage. In conditions such as type 1 diabetes, multiple sclerosis, and rheumatoid arthritis, defects in Treg function or number can lead to a breakdown of tolerance and the development of autoimmunity.

Therapeutic Implications[edit | edit source]

The concept of infectious tolerance has significant implications for the development of immunotherapy strategies. By harnessing the ability of Tregs to induce tolerance, researchers aim to develop treatments for autoimmune diseases, allergies, and transplant rejection. For instance, therapies that expand Treg populations or enhance their function could potentially restore tolerance in patients with autoimmune conditions.

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