Immune Sensitization in the Skin Is Enhanced by Antigen-Independent Effects of IgE
Contact sensitivity responses require both effective immune sensitization following cutaneous exposure to chemical haptens and antigen-specific elicitation of inflammation upon subsequent hapten challenge. We report that antigen-independent effects of IgE antibodies can promote immune sensitization...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2004-04, Vol.20 (4), p.381-392 |
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| creator | Bryce, Paul J Miller, Mendy L Miyajima, Ichiro Tsai, Mindy Galli, Stephen J Oettgen, Hans C |
| description | Contact sensitivity responses require both effective immune sensitization following cutaneous exposure to chemical haptens and antigen-specific elicitation of inflammation upon subsequent hapten challenge. We report that antigen-independent effects of IgE antibodies can promote immune sensitization to haptens in the skin. Contact sensitivity was markedly impaired in IgE
−/− mice but was restored by either transfer of sensitized cells from wild-type mice or administration of hapten-irrelevant IgE before sensitization. Moreover, IgE
−/− mice exhibited impairment in the reduction of dendritic cell numbers in the epidermis after hapten exposure. Monomeric IgE has been reported to influence mast cell function. We observed diminished contact sensitivity in mice lacking FcϵRI or mast cells, and mRNA for several mast cell-associated genes was reduced in IgE
−/− versus wild-type skin after hapten exposure. We speculate that levels of IgE normally present in mice favor immune sensitization via antigen-independent but FcϵRI-dependent effects on mast cells. |
| doi_str_mv | 10.1016/S1074-7613(04)00080-9 |
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−/− mice but was restored by either transfer of sensitized cells from wild-type mice or administration of hapten-irrelevant IgE before sensitization. Moreover, IgE
−/− mice exhibited impairment in the reduction of dendritic cell numbers in the epidermis after hapten exposure. Monomeric IgE has been reported to influence mast cell function. We observed diminished contact sensitivity in mice lacking FcϵRI or mast cells, and mRNA for several mast cell-associated genes was reduced in IgE
−/− versus wild-type skin after hapten exposure. We speculate that levels of IgE normally present in mice favor immune sensitization via antigen-independent but FcϵRI-dependent effects on mast cells.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/S1074-7613(04)00080-9</identifier><identifier>PMID: 15084268</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adjuvants, Immunologic - pharmacology ; Adoptive Transfer ; Allergies ; Animals ; B-Lymphocytes - immunology ; Cell Movement - immunology ; Cytokines ; Defects ; Dendritic Cells - immunology ; Dermatitis, Contact - immunology ; Gene expression ; Haptens - immunology ; Immunization ; Immunoglobulin E - blood ; Immunoglobulin E - immunology ; Mast Cells - immunology ; Mice ; Oxazolone - pharmacology ; Receptors, IgE - immunology ; Reverse Transcriptase Polymerase Chain Reaction ; Skin ; Skin - drug effects ; Skin - immunology ; Skin - pathology ; Variance analysis</subject><ispartof>Immunity (Cambridge, Mass.), 2004-04, Vol.20 (4), p.381-392</ispartof><rights>2004 Cell Press</rights><rights>Copyright Elsevier Limited Apr 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-2f0b68855782b880a4ebc652e61a876021299fc3a873571d74d8b987b29f3e933</citedby><cites>FETCH-LOGICAL-c533t-2f0b68855782b880a4ebc652e61a876021299fc3a873571d74d8b987b29f3e933</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1074761304000809$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15084268$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bryce, Paul J</creatorcontrib><creatorcontrib>Miller, Mendy L</creatorcontrib><creatorcontrib>Miyajima, Ichiro</creatorcontrib><creatorcontrib>Tsai, Mindy</creatorcontrib><creatorcontrib>Galli, Stephen J</creatorcontrib><creatorcontrib>Oettgen, Hans C</creatorcontrib><title>Immune Sensitization in the Skin Is Enhanced by Antigen-Independent Effects of IgE</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>Contact sensitivity responses require both effective immune sensitization following cutaneous exposure to chemical haptens and antigen-specific elicitation of inflammation upon subsequent hapten challenge. We report that antigen-independent effects of IgE antibodies can promote immune sensitization to haptens in the skin. Contact sensitivity was markedly impaired in IgE
−/− mice but was restored by either transfer of sensitized cells from wild-type mice or administration of hapten-irrelevant IgE before sensitization. Moreover, IgE
−/− mice exhibited impairment in the reduction of dendritic cell numbers in the epidermis after hapten exposure. Monomeric IgE has been reported to influence mast cell function. We observed diminished contact sensitivity in mice lacking FcϵRI or mast cells, and mRNA for several mast cell-associated genes was reduced in IgE
−/− versus wild-type skin after hapten exposure. We speculate that levels of IgE normally present in mice favor immune sensitization via antigen-independent but FcϵRI-dependent effects on mast cells.</description><subject>Adjuvants, Immunologic - pharmacology</subject><subject>Adoptive Transfer</subject><subject>Allergies</subject><subject>Animals</subject><subject>B-Lymphocytes - immunology</subject><subject>Cell Movement - immunology</subject><subject>Cytokines</subject><subject>Defects</subject><subject>Dendritic Cells - immunology</subject><subject>Dermatitis, Contact - immunology</subject><subject>Gene expression</subject><subject>Haptens - immunology</subject><subject>Immunization</subject><subject>Immunoglobulin E - blood</subject><subject>Immunoglobulin E - immunology</subject><subject>Mast Cells - immunology</subject><subject>Mice</subject><subject>Oxazolone - pharmacology</subject><subject>Receptors, IgE - immunology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Skin</subject><subject>Skin - drug effects</subject><subject>Skin - immunology</subject><subject>Skin - pathology</subject><subject>Variance analysis</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV1LHDEUhkOpVKv-hJZAodSL0ZOvSXJVZNnWAUHw4zrMx5nd2J3MdjIj6K836y4I3uxNchKec0Kel5BvDM4ZsPzijoGWmc6Z-AXyDAAMZPYTOWJgdSaZgc-beocckq8xPgIwqSx8IYdMgZE8N0fktui6KSC9wxD96F_K0feB-kDHZbr8l4oi0nlYlqHGhlbP9DKMfoEhK0KDa0xLGOm8bbEeI-1bWizmJ-SgLVcRT3f7MXn4M7-fXWXXN3-L2eV1Vishxoy3UOXGKKUNr4yBUmJV54pjzkqjc-CMW9vWIh2E0qzRsjGVNbrithVohTgmP7dz10P_f8I4us7HGlerMmA_RaeZESoX-0GmDUiQKoE_PoCP_TSE9AmXjEnOleEsUWpL1UMf44CtWw--K4dnx8BtsnFv2biNeAfSvWXjbOr7vps-VR027127MBLwewtgsvbkcXCx9rgR74fk1zW93_PEKz7Zmsg</recordid><startdate>20040401</startdate><enddate>20040401</enddate><creator>Bryce, Paul J</creator><creator>Miller, Mendy L</creator><creator>Miyajima, Ichiro</creator><creator>Tsai, Mindy</creator><creator>Galli, Stephen J</creator><creator>Oettgen, Hans C</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20040401</creationdate><title>Immune Sensitization in the Skin Is Enhanced by Antigen-Independent Effects of IgE</title><author>Bryce, Paul J ; 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−/− mice but was restored by either transfer of sensitized cells from wild-type mice or administration of hapten-irrelevant IgE before sensitization. Moreover, IgE
−/− mice exhibited impairment in the reduction of dendritic cell numbers in the epidermis after hapten exposure. Monomeric IgE has been reported to influence mast cell function. We observed diminished contact sensitivity in mice lacking FcϵRI or mast cells, and mRNA for several mast cell-associated genes was reduced in IgE
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| subjects | Adjuvants, Immunologic - pharmacology Adoptive Transfer Allergies Animals B-Lymphocytes - immunology Cell Movement - immunology Cytokines Defects Dendritic Cells - immunology Dermatitis, Contact - immunology Gene expression Haptens - immunology Immunization Immunoglobulin E - blood Immunoglobulin E - immunology Mast Cells - immunology Mice Oxazolone - pharmacology Receptors, IgE - immunology Reverse Transcriptase Polymerase Chain Reaction Skin Skin - drug effects Skin - immunology Skin - pathology Variance analysis |
| title | Immune Sensitization in the Skin Is Enhanced by Antigen-Independent Effects of IgE |
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