Immune responses in a mouse model of vitiligo with spontaneous epidermal de- and repigmentation
Summary To generate a mouse model of spontaneous epidermal depigmentation, parental h3TA2 mice, expressing both a human‐derived, tyrosinase‐reactive T‐cell receptor on T cells and the matching HLA‐A2 transgene, were crossed to keratin 14‐promoter driven, stem cell factor transgenic (K14‐SCF) mice wi...
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| Veröffentlicht in: | Pigment cell and melanoma research 2014-11, Vol.27 (6), p.1075-1085 |
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| creator | Eby, Jonathan M. Kang, Hee-Kap Klarquist, Jared Chatterjee, Shilpak Mosenson, Jeffrey A. Nishimura, Michael I. Garrett-Mayer, Elizabeth Longley, B. Jack Engelhard, Victor H. Mehrotra, Shikhar Le Poole, I. Caroline |
| description | Summary
To generate a mouse model of spontaneous epidermal depigmentation, parental h3TA2 mice, expressing both a human‐derived, tyrosinase‐reactive T‐cell receptor on T cells and the matching HLA‐A2 transgene, were crossed to keratin 14‐promoter driven, stem cell factor transgenic (K14‐SCF) mice with intra‐epidermal melanocytes. In resulting Vitesse mice, spontaneous skin depigmentation precedes symmetrical and sharply demarcated patches of graying hair. Whereas the SCF transgene alone dictates a greater retinoic acid receptor‐related orphan receptor gamma (RORγt)+ T‐cell compartment, these cells displayed markedly increased IL‐17 expression within Vitesse mice. Similar to patient skin, regulatory T cells were less abundant compared with K14‐SCF mice, with the exception of gradually appearing patches of repigmenting skin. The subtle repigmentation observed likely reflects resilient melanocytes that coexist with skin‐infiltrating, melanocyte‐reactive T cells. Similar repigmenting lesions were found in a different TCR transgenic model of vitiligo developed on an SCF transgenic background, supporting a role for SCF in repigmentation. |
| doi_str_mv | 10.1111/pcmr.12284 |
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To generate a mouse model of spontaneous epidermal depigmentation, parental h3TA2 mice, expressing both a human‐derived, tyrosinase‐reactive T‐cell receptor on T cells and the matching HLA‐A2 transgene, were crossed to keratin 14‐promoter driven, stem cell factor transgenic (K14‐SCF) mice with intra‐epidermal melanocytes. In resulting Vitesse mice, spontaneous skin depigmentation precedes symmetrical and sharply demarcated patches of graying hair. Whereas the SCF transgene alone dictates a greater retinoic acid receptor‐related orphan receptor gamma (RORγt)+ T‐cell compartment, these cells displayed markedly increased IL‐17 expression within Vitesse mice. Similar to patient skin, regulatory T cells were less abundant compared with K14‐SCF mice, with the exception of gradually appearing patches of repigmenting skin. The subtle repigmentation observed likely reflects resilient melanocytes that coexist with skin‐infiltrating, melanocyte‐reactive T cells. Similar repigmenting lesions were found in a different TCR transgenic model of vitiligo developed on an SCF transgenic background, supporting a role for SCF in repigmentation.</description><identifier>ISSN: 1755-1471</identifier><identifier>EISSN: 1755-148X</identifier><identifier>DOI: 10.1111/pcmr.12284</identifier><identifier>PMID: 24935676</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animals ; Cell Line ; Disease Models, Animal ; Epidermis - pathology ; Epitopes ; Humans ; Hypopigmentation - complications ; Hypopigmentation - immunology ; Hypopigmentation - pathology ; IL-17 ; Immunity ; Interleukin-17 - metabolism ; Lymphocytes ; Medical research ; Mice, Inbred C57BL ; Mice, Transgenic ; Monophenol Monooxygenase - metabolism ; mouse model ; Pigmentation ; Receptors, Antigen, T-Cell - metabolism ; Rodents ; stem cell factor ; Stem Cell Factor - genetics ; T cell receptors ; T-cell receptor ; T-Lymphocytes, Regulatory - immunology ; Transgenes ; Vitiligo ; Vitiligo - complications ; Vitiligo - immunology ; Vitiligo - pathology</subject><ispartof>Pigment cell and melanoma research, 2014-11, Vol.27 (6), p.1075-1085</ispartof><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2014 John Wiley & Sons A/S</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5564-1a6e52a8f31907fcad3d1945b9986c364b37f6b7474103d9a0cb3a8f62d2beb83</citedby><cites>FETCH-LOGICAL-c5564-1a6e52a8f31907fcad3d1945b9986c364b37f6b7474103d9a0cb3a8f62d2beb83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fpcmr.12284$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fpcmr.12284$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24935676$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eby, Jonathan M.</creatorcontrib><creatorcontrib>Kang, Hee-Kap</creatorcontrib><creatorcontrib>Klarquist, Jared</creatorcontrib><creatorcontrib>Chatterjee, Shilpak</creatorcontrib><creatorcontrib>Mosenson, Jeffrey A.</creatorcontrib><creatorcontrib>Nishimura, Michael I.</creatorcontrib><creatorcontrib>Garrett-Mayer, Elizabeth</creatorcontrib><creatorcontrib>Longley, B. Jack</creatorcontrib><creatorcontrib>Engelhard, Victor H.</creatorcontrib><creatorcontrib>Mehrotra, Shikhar</creatorcontrib><creatorcontrib>Le Poole, I. Caroline</creatorcontrib><title>Immune responses in a mouse model of vitiligo with spontaneous epidermal de- and repigmentation</title><title>Pigment cell and melanoma research</title><addtitle>Pigment Cell Melanoma Res</addtitle><description>Summary
To generate a mouse model of spontaneous epidermal depigmentation, parental h3TA2 mice, expressing both a human‐derived, tyrosinase‐reactive T‐cell receptor on T cells and the matching HLA‐A2 transgene, were crossed to keratin 14‐promoter driven, stem cell factor transgenic (K14‐SCF) mice with intra‐epidermal melanocytes. In resulting Vitesse mice, spontaneous skin depigmentation precedes symmetrical and sharply demarcated patches of graying hair. Whereas the SCF transgene alone dictates a greater retinoic acid receptor‐related orphan receptor gamma (RORγt)+ T‐cell compartment, these cells displayed markedly increased IL‐17 expression within Vitesse mice. Similar to patient skin, regulatory T cells were less abundant compared with K14‐SCF mice, with the exception of gradually appearing patches of repigmenting skin. The subtle repigmentation observed likely reflects resilient melanocytes that coexist with skin‐infiltrating, melanocyte‐reactive T cells. Similar repigmenting lesions were found in a different TCR transgenic model of vitiligo developed on an SCF transgenic background, supporting a role for SCF in repigmentation.</description><subject>Animals</subject><subject>Cell Line</subject><subject>Disease Models, Animal</subject><subject>Epidermis - pathology</subject><subject>Epitopes</subject><subject>Humans</subject><subject>Hypopigmentation - complications</subject><subject>Hypopigmentation - immunology</subject><subject>Hypopigmentation - pathology</subject><subject>IL-17</subject><subject>Immunity</subject><subject>Interleukin-17 - metabolism</subject><subject>Lymphocytes</subject><subject>Medical research</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Monophenol Monooxygenase - metabolism</subject><subject>mouse model</subject><subject>Pigmentation</subject><subject>Receptors, Antigen, T-Cell - metabolism</subject><subject>Rodents</subject><subject>stem cell factor</subject><subject>Stem Cell Factor - genetics</subject><subject>T cell receptors</subject><subject>T-cell receptor</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Transgenes</subject><subject>Vitiligo</subject><subject>Vitiligo - complications</subject><subject>Vitiligo - immunology</subject><subject>Vitiligo - pathology</subject><issn>1755-1471</issn><issn>1755-148X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV9r1TAYh4Mobm7e-AEk4M0QOpPmX3sjyGGbg6ljTOZdSJu3Z5lNU5N2c9_eHLsd1AtzkQTy5Mn75ofQK0oOaR7vxtbHQ1qWFX-CdqkSoqC8-vZ0u1d0B71I6YYQSUTNnqOdktdMSCV3kT71fh4AR0hjGBIk7AZssA9zgjxb6HHo8K2bXO_WAd-56RpvyMkMkBkMo7MQvemxhQKbwWbT6NYeMjG5MOyjZ53pE7x8WPfQ1-Ojy9XH4uzLyenqw1nRCiF5QY0EUZqqY7QmqmuNZZbWXDR1XcmWSd4w1clGccUpYbY2pG1YxmVpywaaiu2h94t3nBsPts3vR9PrMTpv4r0Oxum_TwZ3rdfhVnOuiCJlFhw8CGL4MUOatHephb5fGtVU0oqK_Gsio2_-QW_CHIfc3oYSpawJIZl6u1BtDClF6LbFUKI3uelNbvp3bhl-_Wf5W_QxqAzQBbhzPdz_R6XPV58uHqXFcselCX5u75j4XUvFlNBXn0_0pbg6luJ8pRn7BTfws50</recordid><startdate>201411</startdate><enddate>201411</enddate><creator>Eby, Jonathan M.</creator><creator>Kang, Hee-Kap</creator><creator>Klarquist, Jared</creator><creator>Chatterjee, Shilpak</creator><creator>Mosenson, Jeffrey A.</creator><creator>Nishimura, Michael I.</creator><creator>Garrett-Mayer, Elizabeth</creator><creator>Longley, B. Jack</creator><creator>Engelhard, Victor H.</creator><creator>Mehrotra, Shikhar</creator><creator>Le Poole, I. Caroline</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201411</creationdate><title>Immune responses in a mouse model of vitiligo with spontaneous epidermal de- and repigmentation</title><author>Eby, Jonathan M. ; Kang, Hee-Kap ; Klarquist, Jared ; Chatterjee, Shilpak ; Mosenson, Jeffrey A. ; Nishimura, Michael I. ; Garrett-Mayer, Elizabeth ; Longley, B. Jack ; Engelhard, Victor H. ; Mehrotra, Shikhar ; Le Poole, I. Caroline</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5564-1a6e52a8f31907fcad3d1945b9986c364b37f6b7474103d9a0cb3a8f62d2beb83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Cell Line</topic><topic>Disease Models, Animal</topic><topic>Epidermis - pathology</topic><topic>Epitopes</topic><topic>Humans</topic><topic>Hypopigmentation - complications</topic><topic>Hypopigmentation - immunology</topic><topic>Hypopigmentation - pathology</topic><topic>IL-17</topic><topic>Immunity</topic><topic>Interleukin-17 - metabolism</topic><topic>Lymphocytes</topic><topic>Medical research</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Monophenol Monooxygenase - metabolism</topic><topic>mouse model</topic><topic>Pigmentation</topic><topic>Receptors, Antigen, T-Cell - metabolism</topic><topic>Rodents</topic><topic>stem cell factor</topic><topic>Stem Cell Factor - genetics</topic><topic>T cell receptors</topic><topic>T-cell receptor</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Transgenes</topic><topic>Vitiligo</topic><topic>Vitiligo - complications</topic><topic>Vitiligo - immunology</topic><topic>Vitiligo - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eby, Jonathan M.</creatorcontrib><creatorcontrib>Kang, Hee-Kap</creatorcontrib><creatorcontrib>Klarquist, Jared</creatorcontrib><creatorcontrib>Chatterjee, Shilpak</creatorcontrib><creatorcontrib>Mosenson, Jeffrey A.</creatorcontrib><creatorcontrib>Nishimura, Michael I.</creatorcontrib><creatorcontrib>Garrett-Mayer, Elizabeth</creatorcontrib><creatorcontrib>Longley, B. Jack</creatorcontrib><creatorcontrib>Engelhard, Victor H.</creatorcontrib><creatorcontrib>Mehrotra, Shikhar</creatorcontrib><creatorcontrib>Le Poole, I. Caroline</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Pigment cell and melanoma research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eby, Jonathan M.</au><au>Kang, Hee-Kap</au><au>Klarquist, Jared</au><au>Chatterjee, Shilpak</au><au>Mosenson, Jeffrey A.</au><au>Nishimura, Michael I.</au><au>Garrett-Mayer, Elizabeth</au><au>Longley, B. Jack</au><au>Engelhard, Victor H.</au><au>Mehrotra, Shikhar</au><au>Le Poole, I. Caroline</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immune responses in a mouse model of vitiligo with spontaneous epidermal de- and repigmentation</atitle><jtitle>Pigment cell and melanoma research</jtitle><addtitle>Pigment Cell Melanoma Res</addtitle><date>2014-11</date><risdate>2014</risdate><volume>27</volume><issue>6</issue><spage>1075</spage><epage>1085</epage><pages>1075-1085</pages><issn>1755-1471</issn><eissn>1755-148X</eissn><abstract>Summary
To generate a mouse model of spontaneous epidermal depigmentation, parental h3TA2 mice, expressing both a human‐derived, tyrosinase‐reactive T‐cell receptor on T cells and the matching HLA‐A2 transgene, were crossed to keratin 14‐promoter driven, stem cell factor transgenic (K14‐SCF) mice with intra‐epidermal melanocytes. In resulting Vitesse mice, spontaneous skin depigmentation precedes symmetrical and sharply demarcated patches of graying hair. Whereas the SCF transgene alone dictates a greater retinoic acid receptor‐related orphan receptor gamma (RORγt)+ T‐cell compartment, these cells displayed markedly increased IL‐17 expression within Vitesse mice. Similar to patient skin, regulatory T cells were less abundant compared with K14‐SCF mice, with the exception of gradually appearing patches of repigmenting skin. The subtle repigmentation observed likely reflects resilient melanocytes that coexist with skin‐infiltrating, melanocyte‐reactive T cells. Similar repigmenting lesions were found in a different TCR transgenic model of vitiligo developed on an SCF transgenic background, supporting a role for SCF in repigmentation.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24935676</pmid><doi>10.1111/pcmr.12284</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Cell Line Disease Models, Animal Epidermis - pathology Epitopes Humans Hypopigmentation - complications Hypopigmentation - immunology Hypopigmentation - pathology IL-17 Immunity Interleukin-17 - metabolism Lymphocytes Medical research Mice, Inbred C57BL Mice, Transgenic Monophenol Monooxygenase - metabolism mouse model Pigmentation Receptors, Antigen, T-Cell - metabolism Rodents stem cell factor Stem Cell Factor - genetics T cell receptors T-cell receptor T-Lymphocytes, Regulatory - immunology Transgenes Vitiligo Vitiligo - complications Vitiligo - immunology Vitiligo - pathology |
| title | Immune responses in a mouse model of vitiligo with spontaneous epidermal de- and repigmentation |
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