CD8+ cytolytic T lymphocytes and the skin

: T lymphocytes show a special affinity for the skin. Although the roles played by the CD4+ population of T lymphocytes in immunodermatology were so far actively investigated, much less is known about the roles played in the skin by CD8+ cytolytic T lymphocytes (CTL). The activity of CD8+ CTL in the...

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Veröffentlicht in:Experimental dermatology 1998-08, Vol.7 (4), p.121-131
1. Verfasser: Panfilis, G. De
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description : T lymphocytes show a special affinity for the skin. Although the roles played by the CD4+ population of T lymphocytes in immunodermatology were so far actively investigated, much less is known about the roles played in the skin by CD8+ cytolytic T lymphocytes (CTL). The activity of CD8+ CTL in the immunodermatological context, however, is likely to be most important; the immuno‐biology itself of CD8+ CTL, moreover, although far from being fully understood, shows intriguing characteristics. Immunophenotype, function and cytokine profile of CD8+ CTL are overviewed in the first section of this review. Phenotypically, not only CD8+ CTL can be subdivided into CD8+ CD28+ CD11b+ and CD8+ CD28‐ CD11b+ subsets, but also an up‐to‐now undetected CD8+ CD28‐ CD11b‐ subset does exist. Functionally, not only “cytotoxic” but even “suppressor” subpopulations have been shown to exert cytolytic capabilities indeed, and “suppression” itself may be due to such a lytic capacity. According to cytokine synthesis, CD8+ CTL can be split into Tc1 and Tc2 subsets, each able to influence specific patterns of immune responses. The impact of CD8+ CTL in immunodermatology, overviewed in the second section of the current review, is crucial. The pathophysiology of inflammatory dermatoses is deeply influenced by the activity of CD8+ CTL: e.g., CD8+ CTL within psoriateic epidermis are possibly associated to the persistence of psoriatic lesions not undergoing resolution; on the other hand, in late lesions of lichen planus CD8+ CTL predominate, thus explaining presumably both the cytolytic attack against keratinocytes and the modulation of the inflammatory reaction up to the final resolution of the lesions; Tc1 cells are decreased in atopic dermatitis, and such a decrease can account both for IgE overproduction and for development of infections. Finally, CD8+ CTL can sustain against cutaneous viruses/tumors cytolytic immune responses not only of secondary but even of primary type, i.e. induced by Langerhans cells/dendritic cells either transfected or pulsed with skin virus/tumor‐associated antigens, thus allowing the production of vaccines against cutaneous viral/neoplastic diseases.
doi_str_mv 10.1111/j.1600-0625.1998.tb00312.x
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De</creator><creatorcontrib>Panfilis, G. De</creatorcontrib><description>: T lymphocytes show a special affinity for the skin. Although the roles played by the CD4+ population of T lymphocytes in immunodermatology were so far actively investigated, much less is known about the roles played in the skin by CD8+ cytolytic T lymphocytes (CTL). The activity of CD8+ CTL in the immunodermatological context, however, is likely to be most important; the immuno‐biology itself of CD8+ CTL, moreover, although far from being fully understood, shows intriguing characteristics. Immunophenotype, function and cytokine profile of CD8+ CTL are overviewed in the first section of this review. Phenotypically, not only CD8+ CTL can be subdivided into CD8+ CD28+ CD11b+ and CD8+ CD28‐ CD11b+ subsets, but also an up‐to‐now undetected CD8+ CD28‐ CD11b‐ subset does exist. Functionally, not only “cytotoxic” but even “suppressor” subpopulations have been shown to exert cytolytic capabilities indeed, and “suppression” itself may be due to such a lytic capacity. According to cytokine synthesis, CD8+ CTL can be split into Tc1 and Tc2 subsets, each able to influence specific patterns of immune responses. The impact of CD8+ CTL in immunodermatology, overviewed in the second section of the current review, is crucial. The pathophysiology of inflammatory dermatoses is deeply influenced by the activity of CD8+ CTL: e.g., CD8+ CTL within psoriateic epidermis are possibly associated to the persistence of psoriatic lesions not undergoing resolution; on the other hand, in late lesions of lichen planus CD8+ CTL predominate, thus explaining presumably both the cytolytic attack against keratinocytes and the modulation of the inflammatory reaction up to the final resolution of the lesions; Tc1 cells are decreased in atopic dermatitis, and such a decrease can account both for IgE overproduction and for development of infections. 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De</creatorcontrib><title>CD8+ cytolytic T lymphocytes and the skin</title><title>Experimental dermatology</title><addtitle>Exp Dermatol</addtitle><description>: T lymphocytes show a special affinity for the skin. Although the roles played by the CD4+ population of T lymphocytes in immunodermatology were so far actively investigated, much less is known about the roles played in the skin by CD8+ cytolytic T lymphocytes (CTL). The activity of CD8+ CTL in the immunodermatological context, however, is likely to be most important; the immuno‐biology itself of CD8+ CTL, moreover, although far from being fully understood, shows intriguing characteristics. Immunophenotype, function and cytokine profile of CD8+ CTL are overviewed in the first section of this review. Phenotypically, not only CD8+ CTL can be subdivided into CD8+ CD28+ CD11b+ and CD8+ CD28‐ CD11b+ subsets, but also an up‐to‐now undetected CD8+ CD28‐ CD11b‐ subset does exist. Functionally, not only “cytotoxic” but even “suppressor” subpopulations have been shown to exert cytolytic capabilities indeed, and “suppression” itself may be due to such a lytic capacity. According to cytokine synthesis, CD8+ CTL can be split into Tc1 and Tc2 subsets, each able to influence specific patterns of immune responses. The impact of CD8+ CTL in immunodermatology, overviewed in the second section of the current review, is crucial. The pathophysiology of inflammatory dermatoses is deeply influenced by the activity of CD8+ CTL: e.g., CD8+ CTL within psoriateic epidermis are possibly associated to the persistence of psoriatic lesions not undergoing resolution; on the other hand, in late lesions of lichen planus CD8+ CTL predominate, thus explaining presumably both the cytolytic attack against keratinocytes and the modulation of the inflammatory reaction up to the final resolution of the lesions; Tc1 cells are decreased in atopic dermatitis, and such a decrease can account both for IgE overproduction and for development of infections. Finally, CD8+ CTL can sustain against cutaneous viruses/tumors cytolytic immune responses not only of secondary but even of primary type, i.e. induced by Langerhans cells/dendritic cells either transfected or pulsed with skin virus/tumor‐associated antigens, thus allowing the production of vaccines against cutaneous viral/neoplastic diseases.</description><subject>AIDS/HIV</subject><subject>Animals</subject><subject>anti-tumor cytolytic immune responses</subject><subject>atopic dermatitis</subject><subject>CD11 Antigens - immunology</subject><subject>CD11b</subject><subject>CD28</subject><subject>CD8+ cytolytic T lymphocytes</subject><subject>CD8+ cytotoxic cells</subject><subject>CD8+ suppressor cells</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>Cytotoxicity, Immunologic</subject><subject>Humans</subject><subject>immunodermatology</subject><subject>Immunophenotyping</subject><subject>immunotherapy</subject><subject>lichen planus</subject><subject>psoriasis</subject><subject>SALT</subject><subject>SIS</subject><subject>Skin - immunology</subject><subject>T lymphocytes</subject><subject>Tc1</subject><subject>Tc2</subject><issn>0906-6705</issn><issn>1600-0625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkUFLwzAUx4Moc04_glA8CCKtL02bNB4E2eYUhnqYKF5CmqasW7vOpsP125vSsru5PMj_vV_C7yF0hcHD9tytPEwBXKB-6GHOI6-OAQj2vf0RGh6iYzQEDtSlDMJTdGbMCgAzwsIBGnAWRgHQIboZT6JbRzV1mTd1ppyFkzfFdlnaG20cuUmceqkds8425-gklbnRF30doY-n6WL87M7fZi_jx7mrAmDYTaWUlCSxlpyoIEnSBCiONVeKsjhIZaQ1pJwAsX-JIsJJkFBK05AHPuOSRmSErjvutip_dtrUosiM0nkuN7rcGcEIDzmmgW287xpVVRpT6VRsq6yQVSMwiNaTWIlWhmhliNaT6D2JvR2-7F_ZxYVODqO9GJs_dPlvluvmH2Qx_ZpgH1uA2wEyU-v9ASCrtaDtEsTn60ywkAXfCwt6J3-_RoUZ</recordid><startdate>199808</startdate><enddate>199808</enddate><creator>Panfilis, G. De</creator><general>Blackwell Publishing Ltd</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>7X8</scope></search><sort><creationdate>199808</creationdate><title>CD8+ cytolytic T lymphocytes and the skin</title><author>Panfilis, G. De</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4071-faaa63dbea93c4ddfd061be9cc67b4fa8ee0f9303017883934d666f594279a683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>AIDS/HIV</topic><topic>Animals</topic><topic>anti-tumor cytolytic immune responses</topic><topic>atopic dermatitis</topic><topic>CD11 Antigens - immunology</topic><topic>CD11b</topic><topic>CD28</topic><topic>CD8+ cytolytic T lymphocytes</topic><topic>CD8+ cytotoxic cells</topic><topic>CD8+ suppressor cells</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>Cytotoxicity, Immunologic</topic><topic>Humans</topic><topic>immunodermatology</topic><topic>Immunophenotyping</topic><topic>immunotherapy</topic><topic>lichen planus</topic><topic>psoriasis</topic><topic>SALT</topic><topic>SIS</topic><topic>Skin - immunology</topic><topic>T lymphocytes</topic><topic>Tc1</topic><topic>Tc2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Panfilis, G. De</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>MEDLINE - Academic</collection><jtitle>Experimental dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Panfilis, G. De</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD8+ cytolytic T lymphocytes and the skin</atitle><jtitle>Experimental dermatology</jtitle><addtitle>Exp Dermatol</addtitle><date>1998-08</date><risdate>1998</risdate><volume>7</volume><issue>4</issue><spage>121</spage><epage>131</epage><pages>121-131</pages><issn>0906-6705</issn><eissn>1600-0625</eissn><abstract>: T lymphocytes show a special affinity for the skin. Although the roles played by the CD4+ population of T lymphocytes in immunodermatology were so far actively investigated, much less is known about the roles played in the skin by CD8+ cytolytic T lymphocytes (CTL). The activity of CD8+ CTL in the immunodermatological context, however, is likely to be most important; the immuno‐biology itself of CD8+ CTL, moreover, although far from being fully understood, shows intriguing characteristics. Immunophenotype, function and cytokine profile of CD8+ CTL are overviewed in the first section of this review. Phenotypically, not only CD8+ CTL can be subdivided into CD8+ CD28+ CD11b+ and CD8+ CD28‐ CD11b+ subsets, but also an up‐to‐now undetected CD8+ CD28‐ CD11b‐ subset does exist. Functionally, not only “cytotoxic” but even “suppressor” subpopulations have been shown to exert cytolytic capabilities indeed, and “suppression” itself may be due to such a lytic capacity. According to cytokine synthesis, CD8+ CTL can be split into Tc1 and Tc2 subsets, each able to influence specific patterns of immune responses. The impact of CD8+ CTL in immunodermatology, overviewed in the second section of the current review, is crucial. The pathophysiology of inflammatory dermatoses is deeply influenced by the activity of CD8+ CTL: e.g., CD8+ CTL within psoriateic epidermis are possibly associated to the persistence of psoriatic lesions not undergoing resolution; on the other hand, in late lesions of lichen planus CD8+ CTL predominate, thus explaining presumably both the cytolytic attack against keratinocytes and the modulation of the inflammatory reaction up to the final resolution of the lesions; Tc1 cells are decreased in atopic dermatitis, and such a decrease can account both for IgE overproduction and for development of infections. Finally, CD8+ CTL can sustain against cutaneous viruses/tumors cytolytic immune responses not only of secondary but even of primary type, i.e. induced by Langerhans cells/dendritic cells either transfected or pulsed with skin virus/tumor‐associated antigens, thus allowing the production of vaccines against cutaneous viral/neoplastic diseases.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9758406</pmid><doi>10.1111/j.1600-0625.1998.tb00312.x</doi><tpages>11</tpages></addata></record>
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subjects AIDS/HIV
Animals
anti-tumor cytolytic immune responses
atopic dermatitis
CD11 Antigens - immunology
CD11b
CD28
CD8+ cytolytic T lymphocytes
CD8+ cytotoxic cells
CD8+ suppressor cells
CD8-Positive T-Lymphocytes - immunology
Cytotoxicity, Immunologic
Humans
immunodermatology
Immunophenotyping
immunotherapy
lichen planus
psoriasis
SALT
SIS
Skin - immunology
T lymphocytes
Tc1
Tc2
title CD8+ cytolytic T lymphocytes and the skin
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