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- Publisher Website: 10.1002/eji.1830240947
- Scopus: eid_2-s2.0-0028059929
- PMID: 7916298
- WOS: WOS:A1994PJ30000046
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Article: Experimental allergic encephalomyelitis (EAE) in mice lacking CD4+ T cells
Title | Experimental allergic encephalomyelitis (EAE) in mice lacking CD4<sup>+</sup> T cells |
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Authors | |
Keywords | Knockout mice CD4 Experimental allergic encephalomyelitis |
Issue Date | 1994 |
Citation | European Journal of Immunology, 1994, v. 24, n. 9, p. 2250-2253 How to Cite? |
Abstract | Like most experimental autoimmune disease experimental allergic encephalomyelitis (EAE) has been shown to be mediated by CD4+ helper T cells. In vivo antibody blocking studies with anti‐CD4 and adoptive transfer of activated CD4+ T cells indicate the importance of CD4+ cells in disease induction. Fourth backcross generation mutant CD4—/— PL/J mice were immunized with myelin basic protein. Despite the lack CD4+ T cells some of these mice developed EAE, albeit, at a considerably reduced frequency and with variable severity. Furthermore, antigen‐specific T cell proliferation can be demonstrated, indicating some residual helper activity that is major histocompatibility complex class II restricted. This demonstrates that, although the CD4+ T cell is the prime effector cell in EAE, in mice developmentally lacking in CD4, the expanded double‐negative T cells may subserve helper and effector functions. Copyright © 1994 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim |
Persistent Identifier | http://hdl.handle.net/10722/292431 |
ISSN | 2023 Impact Factor: 4.5 2023 SCImago Journal Rankings: 1.627 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Koh, Dow‐Rhoon ‐R | - |
dc.contributor.author | Ho, Alexandra | - |
dc.contributor.author | Rahemtulla, Amin | - |
dc.contributor.author | Penninger, Josef | - |
dc.contributor.author | Mak, Tak‐Wah ‐W | - |
dc.date.accessioned | 2020-11-17T14:56:28Z | - |
dc.date.available | 2020-11-17T14:56:28Z | - |
dc.date.issued | 1994 | - |
dc.identifier.citation | European Journal of Immunology, 1994, v. 24, n. 9, p. 2250-2253 | - |
dc.identifier.issn | 0014-2980 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292431 | - |
dc.description.abstract | Like most experimental autoimmune disease experimental allergic encephalomyelitis (EAE) has been shown to be mediated by CD4+ helper T cells. In vivo antibody blocking studies with anti‐CD4 and adoptive transfer of activated CD4+ T cells indicate the importance of CD4+ cells in disease induction. Fourth backcross generation mutant CD4—/— PL/J mice were immunized with myelin basic protein. Despite the lack CD4+ T cells some of these mice developed EAE, albeit, at a considerably reduced frequency and with variable severity. Furthermore, antigen‐specific T cell proliferation can be demonstrated, indicating some residual helper activity that is major histocompatibility complex class II restricted. This demonstrates that, although the CD4+ T cell is the prime effector cell in EAE, in mice developmentally lacking in CD4, the expanded double‐negative T cells may subserve helper and effector functions. Copyright © 1994 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim | - |
dc.language | eng | - |
dc.relation.ispartof | European Journal of Immunology | - |
dc.subject | Knockout mice | - |
dc.subject | CD4 | - |
dc.subject | Experimental allergic encephalomyelitis | - |
dc.title | Experimental allergic encephalomyelitis (EAE) in mice lacking CD4<sup>+</sup> T cells | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/eji.1830240947 | - |
dc.identifier.pmid | 7916298 | - |
dc.identifier.scopus | eid_2-s2.0-0028059929 | - |
dc.identifier.volume | 24 | - |
dc.identifier.issue | 9 | - |
dc.identifier.spage | 2250 | - |
dc.identifier.epage | 2253 | - |
dc.identifier.eissn | 1521-4141 | - |
dc.identifier.isi | WOS:A1994PJ30000046 | - |
dc.identifier.issnl | 0014-2980 | - |