pubmed-article:11470767 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11470767 | lifeskim:mentions | umls-concept:C0023270 | lld:lifeskim |
pubmed-article:11470767 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
pubmed-article:11470767 | lifeskim:mentions | umls-concept:C0025919 | lld:lifeskim |
pubmed-article:11470767 | lifeskim:mentions | umls-concept:C0054871 | lld:lifeskim |
pubmed-article:11470767 | lifeskim:mentions | umls-concept:C0301872 | lld:lifeskim |
pubmed-article:11470767 | lifeskim:mentions | umls-concept:C1999216 | lld:lifeskim |
pubmed-article:11470767 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:11470767 | pubmed:dateCreated | 2001-7-25 | lld:pubmed |
pubmed-article:11470767 | pubmed:abstractText | Prior to the activation of CD4 (+) T cells, exogenous proteins must be digested by endo/lysosomal enzymes in antigen-presenting cells (APC) to produce antigenic peptides that are able to be presented on class II molecules of the MHC. Studies described here inspect the functional significance of cathepsin L inhibition for antigen processing and T (h) 1/T (h) 2 differentiation in experimental leishmaniasis. We first demonstrated using in vitro systems that cathepsin L is one of the candidate endo/lysosomal enzymes in processing of soluble Leishmania antigen (SLA) and that its specific inhibitor, CLIK148, modulated the processing of SLA. BALB/c mice are known to be susceptible to infection with Leishmania major. Interestingly, treatment of BALB/c mice with CLIK148 exacerbated the infection by enhancing the development of SLA-specific T (h) 2-type response such as production of IL-4 and generation of T (h) 2-dependent specific IgE/IgG1 antibodies. Moreover, addition of CLIK148 in incubation of a SLA-specific CD4 (+) T cell line with APC up-regulated the production of IL-4. However, CLIK148 did not exert any direct influence on the function of T cells themselves. Taken together, these findings suggest that treatment of host mice with CLIK148 affects the processing of SLA in APC, resulting in the potentiation of T (h) 2-type immune responses and thus leading to exacerbation of the infection. Furthermore, endo/lysosomal cathepsin L was found to be functionally distinct from previously described cathepsins B and D. | lld:pubmed |
pubmed-article:11470767 | pubmed:language | eng | lld:pubmed |
pubmed-article:11470767 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11470767 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11470767 | pubmed:month | Aug | lld:pubmed |
pubmed-article:11470767 | pubmed:issn | 0953-8178 | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:NakanoYY | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:KatunumaNN | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:SakaiTT | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:IshiiKK | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:BUDADD | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:HimenoKK | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:MaekawaYY | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:ZhangTT | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:HisaedaHH | lld:pubmed |
pubmed-article:11470767 | pubmed:author | pubmed-author:DainichiTT | lld:pubmed |
pubmed-article:11470767 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11470767 | pubmed:volume | 13 | lld:pubmed |
pubmed-article:11470767 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11470767 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11470767 | pubmed:pagination | 975-82 | lld:pubmed |
pubmed-article:11470767 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:11470767 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11470767 | pubmed:articleTitle | Treatment with cathepsin L inhibitor potentiates Th2-type immune response in Leishmania major-infected BALB/c mice. | lld:pubmed |
pubmed-article:11470767 | pubmed:affiliation | Department of Parasitology and Immunology, The University of Tokushima School of Medicine, 3 Kuramoto-cho, Tokushima 770-8503, Japan. | lld:pubmed |
pubmed-article:11470767 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11470767 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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