File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Regulatory role of OX22high T cells in mercury-induced autoimmunity in the brown Norway rat

TitleRegulatory role of OX22high T cells in mercury-induced autoimmunity in the brown Norway rat
Authors
Issue Date1993
Citation
Journal of Experimental Medicine, 1993, v. 177 n. 5, p. 1309-1316 How to Cite?
AbstractThe monoclonal antibody OX22 defines a functional split within CD4+ T cells in the rat, with OX22high cells mainly producing interleukin 2 (IL-2) and interferon γ and responsible for delayed-type hypersensitivity responses, and OX22low cells mainly producing IL-4 and -5 and responsible for providing B cell help. There are reciprocal interactions between OX22high and OX22low cells, and it has been suggested that the OX22low subset has a role in the prevention of autoimmunity. We have used OX22 in vivo to define the role of these subsets in mercuric chloride-induced autoimmunity in the Brown Norway rat. In this model, there is polyclonal B cell activation and animals develop widespread tissue injury. Treatment of thymectomized animals with OX22 led to a profound reduction in the number of OX22high T cells in the peripheral blood. OX22-treated animals consistently developed more severe tissue injury than controls given an irrelevant antibody of the same isotype. Control animals pretreated with broad spectrum antimicrobial drugs showed milder tissue injury, but this protective effect of antimicrobials was lost in OX22-treated animals. Transfer of naive T cells to OX22-treated animals provided protection, but if T cells were depleted in vitro of OX22high cells before transfer, this effect was lost. These data provide evidence for a protective immunoregulatory role for OX22high T cells in mercuric chloride-induced autoimmunity.
Persistent Identifierhttp://hdl.handle.net/10722/195422
ISSN
2015 Impact Factor: 11.24
2015 SCImago Journal Rankings: 10.762
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMathieson, PW-
dc.contributor.authorThiru, S-
dc.contributor.authorOliveira, DBG-
dc.date.accessioned2014-02-28T06:12:08Z-
dc.date.available2014-02-28T06:12:08Z-
dc.date.issued1993-
dc.identifier.citationJournal of Experimental Medicine, 1993, v. 177 n. 5, p. 1309-1316-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/195422-
dc.description.abstractThe monoclonal antibody OX22 defines a functional split within CD4+ T cells in the rat, with OX22high cells mainly producing interleukin 2 (IL-2) and interferon γ and responsible for delayed-type hypersensitivity responses, and OX22low cells mainly producing IL-4 and -5 and responsible for providing B cell help. There are reciprocal interactions between OX22high and OX22low cells, and it has been suggested that the OX22low subset has a role in the prevention of autoimmunity. We have used OX22 in vivo to define the role of these subsets in mercuric chloride-induced autoimmunity in the Brown Norway rat. In this model, there is polyclonal B cell activation and animals develop widespread tissue injury. Treatment of thymectomized animals with OX22 led to a profound reduction in the number of OX22high T cells in the peripheral blood. OX22-treated animals consistently developed more severe tissue injury than controls given an irrelevant antibody of the same isotype. Control animals pretreated with broad spectrum antimicrobial drugs showed milder tissue injury, but this protective effect of antimicrobials was lost in OX22-treated animals. Transfer of naive T cells to OX22-treated animals provided protection, but if T cells were depleted in vitro of OX22high cells before transfer, this effect was lost. These data provide evidence for a protective immunoregulatory role for OX22high T cells in mercuric chloride-induced autoimmunity.-
dc.languageeng-
dc.relation.ispartofJournal of Experimental Medicine-
dc.titleRegulatory role of OX22high T cells in mercury-induced autoimmunity in the brown Norway rat-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1084/jem.177.5.1309-
dc.identifier.pmid8478610-
dc.identifier.scopuseid_2-s2.0-0027339525-
dc.identifier.volume177-
dc.identifier.issue5-
dc.identifier.spage1309-
dc.identifier.epage1316-
dc.identifier.isiWOS:A1993KY84900009-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats