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Immune tolerance is a crucial physiological process that enables the immune system to distinguish between harmful pathogens and the body's own tissues. This mechanism is essential for preventing autoimmune diseases, where the immune system mistakenly attacks healthy cells.
At AnyGenes, we provide innovative solutions for studying immune tolerance, including specialized qPCR arrays designed to analyze gene expression profiles associated with tolerance mechanisms. Our products enable researchers to explore the intricate balance between immune activation and tolerance, ultimately paving the way for advanced therapeutic strategies.
The mechanism of T cell tolerance. Central tolerance of T cells occurs in the thymus. Hematopoietic lymphoid progenitors migrate to cortex, where they are screened by thymic epithelia cells and develop into CD4+CD8+ double-positive (DP) thymocytes expressing the T-cell antigen receptor (TCR). DP cells migrate to the medulla. After screening for the ability to bind to self-peptide-associated major histocompatibility complex class I (MHC-I) or MHC class II (MHC-II) molecules on the antigen-presenting cell (APC) surface, DP cells develop into CD4+CD8+ DP thymocytes expressing the TCR. Screening for binding capacity of molecules culminating in Treg CD8+ T cells, and CD4+ T cells migrate to lymph node to undergo peripheral tolerance.
Peripheral tolerance mechanisms, such as exhaustion, deletion, anergy, and regulation are mainly relied upon to suppress the activity of self-reactive T cells. Exhaustion and deletion are realized through inhibiting cell function or proliferative capacity of effector T cell and apoptosis. Anergy describes a state of hyporesponsiveness of naive T cells to TCR stimuli after exposure to antigen. Treg cells regulate by inhibiting effector T cell activity and B cell proliferation via interleukin-(IL)-10, Transforming growth factor-β (TGF-beta), and IL-35.
Anergy refers to the state in which T cells become functionally inactive upon encountering self-antigens without the necessary costimulatory signals.
Regulatory T cells (Tregs), particularly those expressing the transcription factor FOXP3, play a pivotal role in maintaining immunological tolerance and preventing autoimmunity. These cells are essential for distinguishing between self and non-self antigens, thereby regulating immune responses to avoid harmful reactions against the body’s own tissues.
Tregs produce several immunosuppressive cytokines, including IL-10, TGF-β, and IL-35, which inhibit the activation and proliferation of effector T cells (Teff) and other immune cells. This cytokine secretion helps create an environment conducive to immunological tolerance and limits inflammatory responses.
THe proper functioning of Tregs is critical for preventing autoimmune diseases. A deficiency or dysfunction in Tregs can lead to a breakdown of self-tolerance, resulting in conditions such as rheumatoid arthritis, type 1 diabetes, and multiple sclerosis. Studies have shown that individuals with autoimmune diseases often exhibit reduced numbers or impaired function of Tregs, highlighting their protective role in immune regulation.
Recent advancements in immunotherapy aim to restore or enhance immune tolerance through various strategies:
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