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Article: Selective expression of a stable cell surface molecule on type 2 but not type 1 helper T cells

TitleSelective expression of a stable cell surface molecule on type 2 but not type 1 helper T cells
Authors
Issue Date1998
Citation
Journal of Experimental Medicine, 1998, v. 187, n. 5, p. 787-794 How to Cite?
AbstractT helper cell type 1 (Th1) and 2 (Th2) are central to immune regulation. However, no stable cell surface marker capable of distinguishing and separating these two subsets of CD4 + cells has yet been found. Using differential display PCR, we have identified a gene encoding a cell membrane bound molecule, originally designated ST2L, T1, DER4, or Fit, expressed constitutively and stably on the surface of murine Th2s, but not Th1s even after stimulation with a range of immunological stimuli. Antibody against a peptide derived from ST2L strongly and stably labeled the surface of cloned Th2s but not Th1s, and Th2s but not Th1s derived from naive T cells of ovalbumin T cell receptor-α/β transgenic mice. Three-color single cell flow cytometric analysis shows that cell surface ST2L coexpressed with intracellular interleukin (IL)-4, but not with interferon (IFN)-γ. The antibody selectively lysed Th2s in vitro in a complement-dependent manner. In vivo, it enhanced Th1 responses by increasing IFN-γ production and decreasing IL-4 and IL-5 synthesis. It induced resistance to Leishmania major infection in BALB/c mice and exacerbated collagen-induced arthritis in DBA/1 mice. Thus, ST2L is a stable marker distinguishing Th2s from Th1s and is also associated with Th2 functions. Hence, it may be a target for therapeutic intervention.
Persistent Identifierhttp://hdl.handle.net/10722/199907
ISSN
2015 Impact Factor: 11.24
2015 SCImago Journal Rankings: 10.762
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXu, Damo-
dc.contributor.authorChan, WoonLing-
dc.contributor.authorLeung, Bernard-
dc.contributor.authorHuang, Fangping-
dc.contributor.authorWheeler, Rachel D.-
dc.contributor.authorPiedrafita, David M.-
dc.contributor.authorRobinson, John H.-
dc.contributor.authorLiew, Fooyew-
dc.date.accessioned2014-07-26T23:10:53Z-
dc.date.available2014-07-26T23:10:53Z-
dc.date.issued1998-
dc.identifier.citationJournal of Experimental Medicine, 1998, v. 187, n. 5, p. 787-794-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/199907-
dc.description.abstractT helper cell type 1 (Th1) and 2 (Th2) are central to immune regulation. However, no stable cell surface marker capable of distinguishing and separating these two subsets of CD4 + cells has yet been found. Using differential display PCR, we have identified a gene encoding a cell membrane bound molecule, originally designated ST2L, T1, DER4, or Fit, expressed constitutively and stably on the surface of murine Th2s, but not Th1s even after stimulation with a range of immunological stimuli. Antibody against a peptide derived from ST2L strongly and stably labeled the surface of cloned Th2s but not Th1s, and Th2s but not Th1s derived from naive T cells of ovalbumin T cell receptor-α/β transgenic mice. Three-color single cell flow cytometric analysis shows that cell surface ST2L coexpressed with intracellular interleukin (IL)-4, but not with interferon (IFN)-γ. The antibody selectively lysed Th2s in vitro in a complement-dependent manner. In vivo, it enhanced Th1 responses by increasing IFN-γ production and decreasing IL-4 and IL-5 synthesis. It induced resistance to Leishmania major infection in BALB/c mice and exacerbated collagen-induced arthritis in DBA/1 mice. Thus, ST2L is a stable marker distinguishing Th2s from Th1s and is also associated with Th2 functions. Hence, it may be a target for therapeutic intervention.-
dc.languageeng-
dc.relation.ispartofJournal of Experimental Medicine-
dc.titleSelective expression of a stable cell surface molecule on type 2 but not type 1 helper T cells-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1084/jem.187.5.787-
dc.identifier.pmid9480988-
dc.identifier.scopuseid_2-s2.0-2642610290-
dc.identifier.volume187-
dc.identifier.issue5-
dc.identifier.spage787-
dc.identifier.epage794-
dc.identifier.isiWOS:000072444700013-

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