{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T03:12:25Z","timestamp":1792811545499,"version":"4.5.0"},"reference-count":247,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2021,7,21]],"date-time":"2021-07-21T00:00:00Z","timestamp":1626825600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Medicinal Research Reviews"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The sesquiterpene lactone artemisinin from\n                    <jats:italic>Artemisia annua<\/jats:italic>\n                    L. is well established for malaria therapy, but its bioactivity spectrum is much broader. In this review, we give a comprehensive and timely overview of the literature regarding the immunosuppressive activity of artemisinin\u2010type compounds toward inflammatory and autoimmune diseases. Numerous receptor\u2010coupled signaling pathways are inhibited by artemisinins, including the receptors for interleukin\u20101 (IL\u20101), tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1), \u03b23\u2010integrin, or RANKL, toll\u2010like receptors and growth factor receptors. Among the receptor\u2010coupled signal transducers are extracellular signal\u2010regulated protein kinase (ERK), c\u2010Jun N\u2010terminal kinase (JNK), phosphatidylinositol\u20104,5\u2010bisphosphate 3\u2010kinase (PI3K), AKT serine\/threonine kinase (AKT), mitogen\u2010activated protein kinase (MAPK)\/extracellular signal regulated kinase (ERK) kinase (MEK), phospholipase C \u03b31 (PLC\u03b3), and others. All these receptors and signal transduction molecules are known to contribute to the inhibition of the transcription factor nuclear factor \u03ba B (NF\u2010\u03baB). Artemisinins may inhibit NF\u2010\u03baB by silencing these upstream pathways and\/or by direct binding to NF\u2010\u03baB. Numerous NF\u2010\u03baB\u2010regulated downstream genes are downregulated by artemisinin and its derivatives, for example, cytokines, chemokines, and immune receptors, which regulate immune cell differentiation, apoptosis genes, proliferation\u2010regulating genes, signal transducers, and genes involved in antioxidant stress response. In addition to the prominent role of NF\u2010\u03baB, other transcription factors are also inhibited by artemisinins (mammalian target of rapamycin [mTOR], activating protein 1 [AP1]\/FBJ murine osteosarcoma viral oncogene homologue [FOS]\/JUN oncogenic transcription factor [JUN]), hypoxia\u2010induced factor 1\u03b1 (HIF\u20101\u03b1), nuclear factor of activated T cells c1 (NF\u2010ATC1), Signal transducers and activators of transcription (STAT), NF E2\u2010related factor\u20102 (NRF\u20102), retinoic\u2010acid\u2010receptor\u2010related orphan nuclear receptor \u03b3 (ROR\u2010\u03b3t), and forkhead box P\u20103 (FOXP\u20103). Many in vivo experiments in disease\u2010relevant animal models demonstrate therapeutic efficacy of artemisinin\u2010type drugs against rheumatic diseases (rheumatoid arthritis, osteoarthritis, lupus erythematosus, arthrosis, and gout), lung diseases (asthma, acute lung injury,\u00a0and pulmonary fibrosis), neurological diseases (autoimmune encephalitis, Alzheimer's disease, and myasthenia gravis), skin diseases (dermatitis, rosacea, and psoriasis), inflammatory bowel disease, and other inflammatory and autoimmune diseases. Randomized clinical trials should be conducted in the future to translate the plethora of preclinical results into clinical practice.\n                  <\/jats:p>","DOI":"10.1002\/med.21842","type":"journal-article","created":{"date-parts":[[2021,7,21]],"date-time":"2021-07-21T03:52:19Z","timestamp":1626839539000},"page":"3023-3061","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":214,"title":["The immunosuppressive activity of artemisinin\u2010type drugs towards inflammatory and autoimmune diseases"],"prefix":"10.1002","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2637-1681","authenticated-orcid":false,"given":"Thomas","family":"Efferth","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical Biology, Institute of Pharmaceutical and Biomedical Sciences Johannes Gutenberg University  Mainz 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