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Microbial infection stimulates toll-like receptors (TLRs) and other pattern recognition receptors on antigen-presenting cells (APCs), leading to the production of proinflammatory mediators, which in turn can lead to tissue damage. The release of both tissue antigens and bacterial antigens results in bacterial-specific T cells and autoreactive T cells in the process called bystander activation, which contributes to autoimmunity.
