Inflammatory Response & Autoimmunity

Acute inflammation occurs in response to cell damage resulting from infection or injury. During this process, cellular and plasma-derived factors encourage extravasation, the recruitment of circulating immune cells into the affected tissue. These immune cells increase their expression of inflammatory cytokines, recruiting additional immune cells to resolve the infection. The immune response is precisely controlled, and dysregulation of any aspect of the process can result in disease. Chronic inflammation contributes to various pathological and autoimmune conditions including allergy, cardiovascular system disorders, central nervous system disorders, and rheumatoid arthritis. Autoimmunity occurs when immune cells attack the other cells in the same organism. Some immune cell types, such as Th2 cells and alternatively-activated macrophages, promote the allergic response. Recent studies show that inappropriate levels of these cell types can occur during pathological conditions, potentially causing autoimmunity. Analysis of Th2 cell and alternatively-activated macrophage functions during autoimmune responses may identify novel cellular mechanisms that cause these pathophysiological conditions.

QIAGEN provides a broad range of assay technologies for inflammatory response and autoimmunity research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for inflammatory response and autoimmunity studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.