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Renal‐infiltrating CD11c+ cells are pathogenic in murine lupus nephritis through promoting CD4+ T cell responses

Summary Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40–60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in l...

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Published in:Clinical and experimental immunology 2017-11, Vol.190 (2), p.187-200
Main Authors: Liao, X., Ren, J., Reihl, A., Pirapakaran, T., Sreekumar, B., Cecere, T. E., Reilly, C. M., Luo, X. M.
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creator Liao, X.
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description Summary Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40–60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in lupus nephritic kidneys of both SLE patients and lupus‐prone mice. These cells may play important pathogenic or regulatory roles in situ to promote or sustain LN. Here, using lupus‐prone mouse models, we showed the pathogenic role of a kidney‐infiltrating CD11c+ myeloid cell population in LN. These CD11c+ cells accumulated in the kidneys of lupus‐prone mice as LN progressed. Surface markers of this population suggest their dendritic cell identity and differentiation from lymphocyte antigen 6 complex (Ly6C)low mature monocytes. The cytokine/chemokine profile of these renal‐infiltrating CD11c+ cells suggests their roles in promoting LN, which was confirmed further in a loss‐of‐function in‐vivo study by using an antibody‐drug conjugate (ADC) strategy targeting CX3CR1, a chemokine receptor expressed highly on these CD11c+ cells. However, CX3CR1 was dispensable for the homing of CD11c+ cells into lupus nephritic kidneys. Finally, we found that these CD11c+ cells co‐localized with infiltrating T cells in the kidney. Using an ex‐ vivo co‐culture system, we showed that renal‐infiltrating CD11c+ cells promoted the survival, proliferation and interferon‐γ production of renal‐infiltrating CD4+ T cells, suggesting a T cell‐dependent mechanism by which these CD11c+ cells promote LN. Together, our results identify a pathogenic kidney‐infiltrating CD11c+ cell population promoting LN progression, which could be a new therapeutic target for the treatment of LN. A subset of CD11c+ cells accumulates in the lupus nephritic kidneys.These cells possess a phenotype of mature monocyte‐derived dendritic cells. They promote lupus nephritis in vivo and enhance syngeneic renal‐infiltrating CD4+ T cell response ex vivo.
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E. ; Reilly, C. M. ; Luo, X. M.</creator><creatorcontrib>Liao, X. ; Ren, J. ; Reihl, A. ; Pirapakaran, T. ; Sreekumar, B. ; Cecere, T. E. ; Reilly, C. M. ; Luo, X. M.</creatorcontrib><description>Summary Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40–60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in lupus nephritic kidneys of both SLE patients and lupus‐prone mice. These cells may play important pathogenic or regulatory roles in situ to promote or sustain LN. Here, using lupus‐prone mouse models, we showed the pathogenic role of a kidney‐infiltrating CD11c+ myeloid cell population in LN. These CD11c+ cells accumulated in the kidneys of lupus‐prone mice as LN progressed. Surface markers of this population suggest their dendritic cell identity and differentiation from lymphocyte antigen 6 complex (Ly6C)low mature monocytes. The cytokine/chemokine profile of these renal‐infiltrating CD11c+ cells suggests their roles in promoting LN, which was confirmed further in a loss‐of‐function in‐vivo study by using an antibody‐drug conjugate (ADC) strategy targeting CX3CR1, a chemokine receptor expressed highly on these CD11c+ cells. However, CX3CR1 was dispensable for the homing of CD11c+ cells into lupus nephritic kidneys. Finally, we found that these CD11c+ cells co‐localized with infiltrating T cells in the kidney. Using an ex‐ vivo co‐culture system, we showed that renal‐infiltrating CD11c+ cells promoted the survival, proliferation and interferon‐γ production of renal‐infiltrating CD4+ T cells, suggesting a T cell‐dependent mechanism by which these CD11c+ cells promote LN. Together, our results identify a pathogenic kidney‐infiltrating CD11c+ cell population promoting LN progression, which could be a new therapeutic target for the treatment of LN. A subset of CD11c+ cells accumulates in the lupus nephritic kidneys.These cells possess a phenotype of mature monocyte‐derived dendritic cells. They promote lupus nephritis in vivo and enhance syngeneic renal‐infiltrating CD4+ T cell response ex vivo.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/cei.13017</identifier><identifier>PMID: 28722110</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Animal models ; Animals ; Antigens, Ly - immunology ; Autoimmune diseases ; CD11c antigen ; CD11c Antigen - immunology ; CD11c+ cells ; CD4 antigen ; CD4-Positive T-Lymphocytes - immunology ; Cell culture ; Cell Movement ; Cell proliferation ; Chemokines - immunology ; Coculture Techniques ; CX3C Chemokine Receptor 1 ; CX3CR1 ; CX3CR1 protein ; Cytokines - immunology ; Dendritic cells ; Dendritic Cells - immunology ; Disease Models, Animal ; Homing ; Interferon ; Interferon-gamma - biosynthesis ; Interferon-gamma - immunology ; Kidney - immunology ; Kidney - pathology ; Kidneys ; Lupus ; Lupus nephritis ; Lupus Nephritis - immunology ; Lupus Nephritis - physiopathology ; Lymphocytes ; Lymphocytes T ; Mice ; Monocytes ; Morbidity ; MRL/lpr ; Myeloid Cells - immunology ; Myeloid Cells - physiology ; Nephritis ; Original ; Receptors, Chemokine - genetics ; Receptors, Chemokine - metabolism ; Rodents ; Surface markers ; Systemic lupus erythematosus ; T cell receptors ; T cells</subject><ispartof>Clinical and experimental immunology, 2017-11, Vol.190 (2), p.187-200</ispartof><rights>2017 British Society for Immunology</rights><rights>2017 British Society for Immunology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4437-4f95994aaf5fe1025292477e69f0aa3c2328fc45447f864e9e40e488194257fa3</citedby><cites>FETCH-LOGICAL-c4437-4f95994aaf5fe1025292477e69f0aa3c2328fc45447f864e9e40e488194257fa3</cites><orcidid>0000-0002-2809-5836</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5629427/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5629427/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28722110$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liao, X.</creatorcontrib><creatorcontrib>Ren, J.</creatorcontrib><creatorcontrib>Reihl, A.</creatorcontrib><creatorcontrib>Pirapakaran, T.</creatorcontrib><creatorcontrib>Sreekumar, B.</creatorcontrib><creatorcontrib>Cecere, T. E.</creatorcontrib><creatorcontrib>Reilly, C. M.</creatorcontrib><creatorcontrib>Luo, X. M.</creatorcontrib><title>Renal‐infiltrating CD11c+ cells are pathogenic in murine lupus nephritis through promoting CD4+ T cell responses</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40–60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in lupus nephritic kidneys of both SLE patients and lupus‐prone mice. These cells may play important pathogenic or regulatory roles in situ to promote or sustain LN. Here, using lupus‐prone mouse models, we showed the pathogenic role of a kidney‐infiltrating CD11c+ myeloid cell population in LN. These CD11c+ cells accumulated in the kidneys of lupus‐prone mice as LN progressed. Surface markers of this population suggest their dendritic cell identity and differentiation from lymphocyte antigen 6 complex (Ly6C)low mature monocytes. The cytokine/chemokine profile of these renal‐infiltrating CD11c+ cells suggests their roles in promoting LN, which was confirmed further in a loss‐of‐function in‐vivo study by using an antibody‐drug conjugate (ADC) strategy targeting CX3CR1, a chemokine receptor expressed highly on these CD11c+ cells. However, CX3CR1 was dispensable for the homing of CD11c+ cells into lupus nephritic kidneys. Finally, we found that these CD11c+ cells co‐localized with infiltrating T cells in the kidney. Using an ex‐ vivo co‐culture system, we showed that renal‐infiltrating CD11c+ cells promoted the survival, proliferation and interferon‐γ production of renal‐infiltrating CD4+ T cells, suggesting a T cell‐dependent mechanism by which these CD11c+ cells promote LN. Together, our results identify a pathogenic kidney‐infiltrating CD11c+ cell population promoting LN progression, which could be a new therapeutic target for the treatment of LN. A subset of CD11c+ cells accumulates in the lupus nephritic kidneys.These cells possess a phenotype of mature monocyte‐derived dendritic cells. They promote lupus nephritis in vivo and enhance syngeneic renal‐infiltrating CD4+ T cell response ex vivo.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antigens, Ly - immunology</subject><subject>Autoimmune diseases</subject><subject>CD11c antigen</subject><subject>CD11c Antigen - immunology</subject><subject>CD11c+ cells</subject><subject>CD4 antigen</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Cell culture</subject><subject>Cell Movement</subject><subject>Cell proliferation</subject><subject>Chemokines - immunology</subject><subject>Coculture Techniques</subject><subject>CX3C Chemokine Receptor 1</subject><subject>CX3CR1</subject><subject>CX3CR1 protein</subject><subject>Cytokines - immunology</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Disease Models, Animal</subject><subject>Homing</subject><subject>Interferon</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interferon-gamma - immunology</subject><subject>Kidney - immunology</subject><subject>Kidney - pathology</subject><subject>Kidneys</subject><subject>Lupus</subject><subject>Lupus nephritis</subject><subject>Lupus Nephritis - immunology</subject><subject>Lupus Nephritis - physiopathology</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Mice</subject><subject>Monocytes</subject><subject>Morbidity</subject><subject>MRL/lpr</subject><subject>Myeloid Cells - immunology</subject><subject>Myeloid Cells - physiology</subject><subject>Nephritis</subject><subject>Original</subject><subject>Receptors, Chemokine - genetics</subject><subject>Receptors, Chemokine - metabolism</subject><subject>Rodents</subject><subject>Surface markers</subject><subject>Systemic lupus erythematosus</subject><subject>T cell receptors</subject><subject>T cells</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp1kd9qFTEQh4Mo9li98AUk4I1Sts2_TTY3BTlWLRQEqdchxsnZlN1kTXaV3vUR-ow-iTk9x6KCuRnCfHzMzA-h55Qc0_pOHIRjyglVD9CKctk2jAn9EK0IIbrRlIgD9KSUq_qVUrLH6IB1ijFKyQrlTxDt8PPmNkQfhjnbOcQNXr-l1B1hB8NQsM2AJzv3aQMxOBwiHpccIuBhmZaCI0x9DnMoeO5zWjY9nnIa094jjvDlnQdnKFOKBcpT9MjbocCzfT1En9-dXa4_NBcf35-v31w0TgiuGuF1q7Ww1rceKGEt00woBVJ7Yi13jLPOO9EKoXwnBWgQBETXUS1Yq7zlh-h0552WLyN8dRDreoOZchhtvjbJBvN3J4bebNJ300pWHaoKXu0FOX1boMxmDGW7i42QlmKoZoRrITmt6Mt_0Ku05HrZLSUUl13XdpV6vaNcTqVk8PfDUGK2SZqapLlLsrIv_pz-nvwdXQVOdsCPMMD1_01mfXa-U_4Chlyogw</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>Liao, X.</creator><creator>Ren, J.</creator><creator>Reihl, A.</creator><creator>Pirapakaran, T.</creator><creator>Sreekumar, B.</creator><creator>Cecere, T. 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M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4437-4f95994aaf5fe1025292477e69f0aa3c2328fc45447f864e9e40e488194257fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Antigens, Ly - immunology</topic><topic>Autoimmune diseases</topic><topic>CD11c antigen</topic><topic>CD11c Antigen - immunology</topic><topic>CD11c+ cells</topic><topic>CD4 antigen</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Cell culture</topic><topic>Cell Movement</topic><topic>Cell proliferation</topic><topic>Chemokines - immunology</topic><topic>Coculture Techniques</topic><topic>CX3C Chemokine Receptor 1</topic><topic>CX3CR1</topic><topic>CX3CR1 protein</topic><topic>Cytokines - immunology</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - immunology</topic><topic>Disease Models, Animal</topic><topic>Homing</topic><topic>Interferon</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interferon-gamma - immunology</topic><topic>Kidney - immunology</topic><topic>Kidney - pathology</topic><topic>Kidneys</topic><topic>Lupus</topic><topic>Lupus nephritis</topic><topic>Lupus Nephritis - immunology</topic><topic>Lupus Nephritis - physiopathology</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Mice</topic><topic>Monocytes</topic><topic>Morbidity</topic><topic>MRL/lpr</topic><topic>Myeloid Cells - immunology</topic><topic>Myeloid Cells - physiology</topic><topic>Nephritis</topic><topic>Original</topic><topic>Receptors, Chemokine - genetics</topic><topic>Receptors, Chemokine - metabolism</topic><topic>Rodents</topic><topic>Surface markers</topic><topic>Systemic lupus erythematosus</topic><topic>T cell receptors</topic><topic>T cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liao, X.</creatorcontrib><creatorcontrib>Ren, J.</creatorcontrib><creatorcontrib>Reihl, A.</creatorcontrib><creatorcontrib>Pirapakaran, T.</creatorcontrib><creatorcontrib>Sreekumar, B.</creatorcontrib><creatorcontrib>Cecere, T. E.</creatorcontrib><creatorcontrib>Reilly, C. M.</creatorcontrib><creatorcontrib>Luo, X. M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liao, X.</au><au>Ren, J.</au><au>Reihl, A.</au><au>Pirapakaran, T.</au><au>Sreekumar, B.</au><au>Cecere, T. E.</au><au>Reilly, C. M.</au><au>Luo, X. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renal‐infiltrating CD11c+ cells are pathogenic in murine lupus nephritis through promoting CD4+ T cell responses</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2017-11</date><risdate>2017</risdate><volume>190</volume><issue>2</issue><spage>187</spage><epage>200</epage><pages>187-200</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><abstract>Summary Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40–60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in lupus nephritic kidneys of both SLE patients and lupus‐prone mice. These cells may play important pathogenic or regulatory roles in situ to promote or sustain LN. Here, using lupus‐prone mouse models, we showed the pathogenic role of a kidney‐infiltrating CD11c+ myeloid cell population in LN. These CD11c+ cells accumulated in the kidneys of lupus‐prone mice as LN progressed. Surface markers of this population suggest their dendritic cell identity and differentiation from lymphocyte antigen 6 complex (Ly6C)low mature monocytes. The cytokine/chemokine profile of these renal‐infiltrating CD11c+ cells suggests their roles in promoting LN, which was confirmed further in a loss‐of‐function in‐vivo study by using an antibody‐drug conjugate (ADC) strategy targeting CX3CR1, a chemokine receptor expressed highly on these CD11c+ cells. However, CX3CR1 was dispensable for the homing of CD11c+ cells into lupus nephritic kidneys. Finally, we found that these CD11c+ cells co‐localized with infiltrating T cells in the kidney. Using an ex‐ vivo co‐culture system, we showed that renal‐infiltrating CD11c+ cells promoted the survival, proliferation and interferon‐γ production of renal‐infiltrating CD4+ T cells, suggesting a T cell‐dependent mechanism by which these CD11c+ cells promote LN. Together, our results identify a pathogenic kidney‐infiltrating CD11c+ cell population promoting LN progression, which could be a new therapeutic target for the treatment of LN. A subset of CD11c+ cells accumulates in the lupus nephritic kidneys.These cells possess a phenotype of mature monocyte‐derived dendritic cells. They promote lupus nephritis in vivo and enhance syngeneic renal‐infiltrating CD4+ T cell response ex vivo.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>28722110</pmid><doi>10.1111/cei.13017</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-2809-5836</orcidid><oa>free_for_read</oa></addata></record>
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subjects Animal models
Animals
Antigens, Ly - immunology
Autoimmune diseases
CD11c antigen
CD11c Antigen - immunology
CD11c+ cells
CD4 antigen
CD4-Positive T-Lymphocytes - immunology
Cell culture
Cell Movement
Cell proliferation
Chemokines - immunology
Coculture Techniques
CX3C Chemokine Receptor 1
CX3CR1
CX3CR1 protein
Cytokines - immunology
Dendritic cells
Dendritic Cells - immunology
Disease Models, Animal
Homing
Interferon
Interferon-gamma - biosynthesis
Interferon-gamma - immunology
Kidney - immunology
Kidney - pathology
Kidneys
Lupus
Lupus nephritis
Lupus Nephritis - immunology
Lupus Nephritis - physiopathology
Lymphocytes
Lymphocytes T
Mice
Monocytes
Morbidity
MRL/lpr
Myeloid Cells - immunology
Myeloid Cells - physiology
Nephritis
Original
Receptors, Chemokine - genetics
Receptors, Chemokine - metabolism
Rodents
Surface markers
Systemic lupus erythematosus
T cell receptors
T cells
title Renal‐infiltrating CD11c+ cells are pathogenic in murine lupus nephritis through promoting CD4+ T cell responses
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