Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities
Type I interferons (IFNs) are immunostimulatory molecules that can activate the innate and adaptive immune systems. In cases of immune dysfunction, prolonged activation of the type I IFN pathway has been correlated with kidney tissue damage in a wide range of kidney disorders, such as lupus nephriti...
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creator | Tumlin, James Rovin, Brad Anders, Hans-Joachim Mysler, Eduardo F. Jayne, David R.W. Takeuchi, Tsutomu Lindholm, Catharina Weiss, Gudrun Sorrentino, Alessandro Woollard, Kevin Ferrari, Nicola |
description | Type I interferons (IFNs) are immunostimulatory molecules that can activate the innate and adaptive immune systems. In cases of immune dysfunction, prolonged activation of the type I IFN pathway has been correlated with kidney tissue damage in a wide range of kidney disorders, such as lupus nephritis (LN) and focal segmental glomerulosclerosis (FSGS). Genetic mutations, such as APOL1 risk variants in conjunction with elevated type I IFN expression, are also associated with higher rates of chronic kidney disease in patients with LN and collapsing FSGS. Long-term activation of the type I IFN pathway can result in chronic inflammation, leading to kidney tissue damage, cell death, and decline in organ function. Thus, therapeutic strategies targeting type I IFN could provide clinical benefits to patients with immune dysregulation who are at risk of developing impaired kidney function. Here, we present a critical review of type I IFN signaling, the consequences of chronically elevated type I IFN expression, and therapeutic strategies targeting type I IFN signaling in the context of kidney disease. |
doi_str_mv | 10.1016/j.ekir.2024.10.013 |
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In cases of immune dysfunction, prolonged activation of the type I IFN pathway has been correlated with kidney tissue damage in a wide range of kidney disorders, such as lupus nephritis (LN) and focal segmental glomerulosclerosis (FSGS). Genetic mutations, such as APOL1 risk variants in conjunction with elevated type I IFN expression, are also associated with higher rates of chronic kidney disease in patients with LN and collapsing FSGS. Long-term activation of the type I IFN pathway can result in chronic inflammation, leading to kidney tissue damage, cell death, and decline in organ function. Thus, therapeutic strategies targeting type I IFN could provide clinical benefits to patients with immune dysregulation who are at risk of developing impaired kidney function. Here, we present a critical review of type I IFN signaling, the consequences of chronically elevated type I IFN expression, and therapeutic strategies targeting type I IFN signaling in the context of kidney disease.</description><identifier>ISSN: 2468-0249</identifier><identifier>EISSN: 2468-0249</identifier><identifier>DOI: 10.1016/j.ekir.2024.10.013</identifier><identifier>PMID: 39810777</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>anifrolumab ; immune dysfunction ; interferon pathway ; kidney disease ; lupus nephritis ; Review ; type I interferon</subject><ispartof>Kidney international reports, 2025-01, Vol.10 (1), p.29-39</ispartof><rights>2024 International Society of Nephrology</rights><rights>2024 International Society of Nephrology. Published by Elsevier Inc.</rights><rights>2024 International Society of Nephrology. 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In cases of immune dysfunction, prolonged activation of the type I IFN pathway has been correlated with kidney tissue damage in a wide range of kidney disorders, such as lupus nephritis (LN) and focal segmental glomerulosclerosis (FSGS). Genetic mutations, such as APOL1 risk variants in conjunction with elevated type I IFN expression, are also associated with higher rates of chronic kidney disease in patients with LN and collapsing FSGS. Long-term activation of the type I IFN pathway can result in chronic inflammation, leading to kidney tissue damage, cell death, and decline in organ function. Thus, therapeutic strategies targeting type I IFN could provide clinical benefits to patients with immune dysregulation who are at risk of developing impaired kidney function. Here, we present a critical review of type I IFN signaling, the consequences of chronically elevated type I IFN expression, and therapeutic strategies targeting type I IFN signaling in the context of kidney disease.</description><subject>anifrolumab</subject><subject>immune dysfunction</subject><subject>interferon pathway</subject><subject>kidney disease</subject><subject>lupus nephritis</subject><subject>Review</subject><subject>type I interferon</subject><issn>2468-0249</issn><issn>2468-0249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><recordid>eNp9kc1uEzEUhS0EolXpC7BAXrJJ6p-Z8QxCQqjQElGpCIW1dWPfSRwm9mB7ivI2PAtPhqOUqmxY2Tr3nGPrfoS85GzOGW8utnP87uJcMFEVYc64fEJORdW0s6J0Tx_dT8h5SlvGGFdN3bH2OTmRXcuZUuqU-CXENWbn1zRvkC73I9IFXfiMsccYPP0CefMT9tR5ej2EHcZpgEg_O-txTz-4hJDwDf0K2QUPA_7-Bd7S5QYjjDhlZ-jtOIaYJ--yw_SCPOthSHh-f56Rb1cfl5efZje314vL9zczIzqZZ9IYZgCgsZY1FfZ93dmqUdaaTvbCKmlBYKUEQFcZs7KgalYZ0ZacNKu-lWfk3bF3nFY7tAZ9jjDoMbodxL0O4PS_E-82eh3uNOdK1K1gpeH1fUMMPyZMWe9cMjgM4DFMSUte14q3tRTFKo5WE0NKEfuHdzjTB1h6qw-w9AHWQSuwSujV4x8-RP6iKYa3RwOWPd05jDoZh96gdRFN1ja4__X_AfzIqms</recordid><startdate>20250101</startdate><enddate>20250101</enddate><creator>Tumlin, James</creator><creator>Rovin, Brad</creator><creator>Anders, Hans-Joachim</creator><creator>Mysler, Eduardo F.</creator><creator>Jayne, David R.W.</creator><creator>Takeuchi, Tsutomu</creator><creator>Lindholm, Catharina</creator><creator>Weiss, Gudrun</creator><creator>Sorrentino, Alessandro</creator><creator>Woollard, Kevin</creator><creator>Ferrari, Nicola</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5639-0210</orcidid></search><sort><creationdate>20250101</creationdate><title>Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities</title><author>Tumlin, James ; Rovin, Brad ; Anders, Hans-Joachim ; Mysler, Eduardo F. ; Jayne, David R.W. ; Takeuchi, Tsutomu ; Lindholm, Catharina ; Weiss, Gudrun ; Sorrentino, Alessandro ; Woollard, Kevin ; Ferrari, Nicola</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c293t-3cc0caaa6dd064eff59d467ddc93f2d73da2e472aa94ccbda7504c283cc3cbf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2025</creationdate><topic>anifrolumab</topic><topic>immune dysfunction</topic><topic>interferon pathway</topic><topic>kidney disease</topic><topic>lupus nephritis</topic><topic>Review</topic><topic>type I interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tumlin, James</creatorcontrib><creatorcontrib>Rovin, Brad</creatorcontrib><creatorcontrib>Anders, Hans-Joachim</creatorcontrib><creatorcontrib>Mysler, Eduardo F.</creatorcontrib><creatorcontrib>Jayne, David R.W.</creatorcontrib><creatorcontrib>Takeuchi, Tsutomu</creatorcontrib><creatorcontrib>Lindholm, Catharina</creatorcontrib><creatorcontrib>Weiss, Gudrun</creatorcontrib><creatorcontrib>Sorrentino, Alessandro</creatorcontrib><creatorcontrib>Woollard, Kevin</creatorcontrib><creatorcontrib>Ferrari, Nicola</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Kidney international reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tumlin, James</au><au>Rovin, Brad</au><au>Anders, Hans-Joachim</au><au>Mysler, Eduardo F.</au><au>Jayne, David R.W.</au><au>Takeuchi, Tsutomu</au><au>Lindholm, Catharina</au><au>Weiss, Gudrun</au><au>Sorrentino, Alessandro</au><au>Woollard, Kevin</au><au>Ferrari, Nicola</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities</atitle><jtitle>Kidney international reports</jtitle><addtitle>Kidney Int Rep</addtitle><date>2025-01-01</date><risdate>2025</risdate><volume>10</volume><issue>1</issue><spage>29</spage><epage>39</epage><pages>29-39</pages><issn>2468-0249</issn><eissn>2468-0249</eissn><abstract>Type I interferons (IFNs) are immunostimulatory molecules that can activate the innate and adaptive immune systems. In cases of immune dysfunction, prolonged activation of the type I IFN pathway has been correlated with kidney tissue damage in a wide range of kidney disorders, such as lupus nephritis (LN) and focal segmental glomerulosclerosis (FSGS). Genetic mutations, such as APOL1 risk variants in conjunction with elevated type I IFN expression, are also associated with higher rates of chronic kidney disease in patients with LN and collapsing FSGS. Long-term activation of the type I IFN pathway can result in chronic inflammation, leading to kidney tissue damage, cell death, and decline in organ function. Thus, therapeutic strategies targeting type I IFN could provide clinical benefits to patients with immune dysregulation who are at risk of developing impaired kidney function. 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subjects | anifrolumab immune dysfunction interferon pathway kidney disease lupus nephritis Review type I interferon |
title | Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities |
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