{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T02:58:51Z","timestamp":1777517931177,"version":"3.51.4"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2000,1,1]],"date-time":"2000-01-01T00:00:00Z","timestamp":946684800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2000,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Pemphigus vulgaris (PV) is an autoimmune bullous skin disease characterized by Abs to the desmosomal cadherin desmoglein-3. Although the autoantibodies have been shown to be pathogenic, the role of the cellular immune system in the pathology of pemphigus-induced acantholysis is unclear. To further delineate the potential role of T cell-signaling pathways in the pathogenesis of PV, we performed passive transfer experiments with PV IgG in gene-targeted mutant mice. Our results demonstrated that CD28-deficient mice (lacking a costimulatory signal for T cell activation) are 5-fold more sensitive to the development of PV than wild-type mice. To evaluate whether the higher incidence of disease was due to an impairment in intercellular adhesion of keratinocytes, we performed an in vitro acantholysis, using CD28\u2212\/\u2212 mice keratinocytes. No alteration in in vitro adhesion was detected in CD28\u2212\/\u2212-type keratinocytes. Because the CD28 molecule plays a pivotal role in the induction of Th2 cytokines, we examined the levels of a prototypic Th2 cytokine (IL-10) in CD28\u2212\/\u2212 mice. Lower levels of IL-10 mRNA were found in lesions from CD28\u2212\/\u2212 mice. To determine whether pemphigus susceptibility in CD28\u2212\/\u2212 was related to IL-10 deficiency, we performed passive transfer experiments in IL-10\u2212\/\u2212 mice that demonstrated increased blisters compared with controls. To confirm that IL-10 is involved in the pathogenesis, rIL-10 was given with PV IgG. IL-10 significantly suppressed the disease activity. These data suggest a potential role of IL-10 in PV.<\/jats:p>","DOI":"10.4049\/jimmunol.164.1.522","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T18:07:57Z","timestamp":1398103677000},"page":"522-529","source":"Crossref","is-referenced-by-count":40,"title":["Immune Modulation in Pemphigus Vulgaris: Role of CD28 and IL-10"],"prefix":"10.1093","volume":"164","author":[{"given":"Paola","family":"Toto","sequence":"first","affiliation":[{"name":"Department of Dermatology, University \u201c G.d\u2019Annunzio,\u201d \u00a0 Chieti ,","place":["Italy"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Claudio","family":"Feliciani","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University \u201c G.d\u2019Annunzio,\u201d \u00a0 Chieti ,","place":["Italy"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paolo","family":"Amerio","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University \u201c G.d\u2019Annunzio,\u201d \u00a0 Chieti ,","place":["Italy"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hirotake","family":"Suzuki","sequence":"additional","affiliation":[{"name":"University of Toronto , Toronto ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Binghe","family":"Wang","sequence":"additional","affiliation":[{"name":"University of Toronto , Toronto ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gulnar M","family":"Shivji","sequence":"additional","affiliation":[{"name":"University of Toronto , Toronto ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Woodley","sequence":"additional","affiliation":[{"name":"Northwestern University , Chicago, IL 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel N","family":"Sauder","sequence":"additional","affiliation":[{"name":"University of Toronto , Toronto ,","place":["Canada"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2000,1,1]]},"reference":[{"key":"2026020906021061600_R1","first-page":"281","volume-title":"J. 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