Inflammation and Autoimmunity are critical to immune response. Inflammation is a vital biological response that protects the body from harmful stimuli, such as pathogens, damaged cells, and irritants. However, in autoimmune diseases, this protective mechanism can become dysregulated, leading to the immune system mistakenly attacking the body's own tissues. Conditions such as rheumatoid arthritis, lupus, and multiple sclerosis showcase how dysregulated inflammation impacts health.
AnyGenes provides innovative qPCR arrays that support high-throughput analysis of inflammatory and autoimmune markers, offering insights into immune responses and facilitating advancements in autoimmune research. Our customizable arrays enable researchers to explore gene expressions linked to inflammation and autoimmunity across various cell types, enhancing the study of disease mechanisms and potential therapeutic targets.
The pathogenesis of RA. Antigen-presenting cells activate T cells and B cells to trigger adaptive immunity. B cells produce autoantibodies that stimulate macrophages to secrete pro-inflammatory factors and promote transcription of inflammatory genes. T cell differentiation into TH17 cells plays a pro-inflammatory role, and IL-4/IL-13 produced by TH2 cells triggers the activation of anti-inflammatory signaling pathways, and the production of anti-inflammatory factors and anti-inflammatory lipids is conducive to disease reversal. PD1 PD15, anti-inflammatory lipids. APCs, antigen-presenting cells. TCR, T cell receptor. TLR, Toll-like receptor.
Autoimmunity arises when the immune system fails to distinguish between self and non-self, leading to the destruction of healthy tissues. Immune cells, including T cells and B cells, become hyperactive, attacking healthy tissues. This leads to a cycle of chronic inflammation and tissue damage. Researchers are increasingly focusing on how immune tolerance is broken and how signaling pathways can be targeted to restore this balance. Understanding the molecular mechanisms behind immune tolerance and signaling pathways is essential for developing therapeutic strategies.
The relationship between inflammation and autoimmunity is intricate. Chronic inflammation can exacerbate autoimmune responses by promoting the activation of immune cells, such as macrophages and T cells, that target self-tissues. For instance, in conditions like rheumatoid arthritis, inflammatory cytokines such as TNF-α and IL-1β play significant roles in perpetuating the disease process by sustaining inflammation and driving autoimmunity.
Management of autoimmune diseases often focuses on reducing inflammation and modulating the immune response.
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