Figure 2: A defensive inflammatory response starts after the pattern recognition receptors (PRRs) of macrophages and dendritic cells are stimulated by both pathogen-associated molecular patterns (PAMPs) released by microorganisms and damage-associated molecular patterns (DAMPs) from injured tissues. As a consequence, diverse signaling pathways increase both the production of proinflammatory cytokines and the release of free radicals during the cellular respiratory burst. The evolution of the inflammatory response is modulated by various subpopulations of cells including T lymphocytes. The proinflammatory T lymphocytes (Th1 and Th17) mainly release IL-2, IL-17, and IFN-γ, and the antiinflammatory lymphocytes (Treg) release TGF-β and IL-10. The effective modulatory work of Treg cells gradually slows down the progression of the inflammatory responses and reduces any possible risk of autoimmunity, allergies, or other chronic diseases.