Immune system modulation via anti-inflammatory effect

Immune system modulation via anti-inflammatory effect describes a collection of strategies to dampen excessive immune responses central to inflammatory diseases, autoimmunity, and cancer by targeting immune cells like dendritic cells, T cells, macrophages, and neutrophils at sites such as lymph nodes, tumors, or inflamed tissues. This involves biomaterials, nanoparticles, and small molecules that deliver antigens, cytokines, or agonists to promote tolerance or repolarize pro-inflammatory M1 macrophages to anti-inflammatory M2 phenotypes, often via pathways like NF-κB, p38-MAPK, JAK-STAT, or mTOR. In disease contexts, overactive inflammation drives pathology in conditions like rheumatoid arthritis, multiple sclerosis, colitis, and atherosclerosis, where therapies aim to suppress proinflammatory cytokines (e.g., TNF-α, IL-6) or enhance regulatory T cells. Drugs interact indirectly through cell surface receptors or intracellular signaling, with examples including JAK inhibitors like tofacitinib that block cytokine release and monoclonal antibodies neutralizing TNF-α. Challenges include achieving antigen-specific targeting to avoid broad immunosuppression, which risks infections, and ensuring precise delivery to avoid hepatic clearance. Overall, this approach enhances immunotherapy efficacy but lacks a singular molecular target, relying instead on multi-component interventions.

Other names

Anti-inflammatory immune modulationImmunomodulation for inflammation control

Cytokine suppression (e.g., TNF-α, IL-6 inhibition), T-cell activation blockade, mTOR pathway inhibition, JAK-STAT signaling blockade, Inflammasome inhibition (e.g., NLRP3), Immune cell repolarization (M1 to M2)