Please use this identifier to cite or link to this item:
https://doi.org/10.1016/j.it.2004.06.005
DC Field | Value | |
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dc.title | IL-4 in tuberculosis: Implications for vaccine design | |
dc.contributor.author | Rook, G.A.W. | |
dc.contributor.author | Hernandez-Pando, R. | |
dc.contributor.author | Dheda, K. | |
dc.contributor.author | Teng Seah, G. | |
dc.date.accessioned | 2016-11-29T01:22:22Z | |
dc.date.available | 2016-11-29T01:22:22Z | |
dc.date.issued | 2004-09 | |
dc.identifier.citation | Rook, G.A.W., Hernandez-Pando, R., Dheda, K., Teng Seah, G. (2004-09). IL-4 in tuberculosis: Implications for vaccine design. Trends in Immunology 25 (9) : 483-488. ScholarBank@NUS Repository. https://doi.org/10.1016/j.it.2004.06.005 | |
dc.identifier.issn | 14714906 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/131755 | |
dc.description.abstract | Current attempts to find a vaccine for tuberculosis (TB) are based on the assumption that it must drive a Th1 response. We review the evidence that progressive disease might not be due to absence of Th1, but rather to the subversive effect of an unusual Th2-like response, involving interleukin-4 (IL-4) and IL-4δ2. This Th2-like response can impair bactericidal function and lead to toxicity of tumour necrosis factor-α (TNF-α) and to pulmonary fibrosis. If this is important, effective vaccines will need to suppress pre-existing Th2-like activity. Such vaccines are feasible and are active therapeutically in mouse TB. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.it.2004.06.005 | |
dc.source | Scopus | |
dc.type | Review | |
dc.contributor.department | MICROBIOLOGY | |
dc.description.doi | 10.1016/j.it.2004.06.005 | |
dc.description.sourcetitle | Trends in Immunology | |
dc.description.volume | 25 | |
dc.description.issue | 9 | |
dc.description.page | 483-488 | |
dc.description.coden | TIRMA | |
dc.identifier.isiut | 000223871400006 | |
Appears in Collections: | Staff Publications |
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