| pubmed-article:10684864 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C0521066 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C1167395 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C1522604 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C0032214 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C1545588 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C1621857 | lld:lifeskim |
| pubmed-article:10684864 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:10684864 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10684864 | pubmed:dateCreated | 2000-4-19 | lld:pubmed |
| pubmed-article:10684864 | pubmed:abstractText | Host defense against multicellular, extracellular pathogens such as nematode parasites is believed to be mediated largely, if not exclusively, by T lymphocytes. During our investigations into the course of Brugia malayi and Brugia pahangi infections in immunodeficient mouse models, we found that mice lacking B lymphocytes were permissive for Brugian infections, whereas immunocompetent mice were uniformly resistant. Mice bearing the Btk(xid) mutation were as permissive as those lacking all B cells, suggesting that the B1 subset may be responsible for host protection. Reconstitution of immunodeficient recombination activating gene (Rag)-1(-/)- mice with B1 B cells conferred resistance, even in the absence of conventional B2 lymphocytes and most T cells. These results suggest that B1 B cells are necessary to mediate host resistance to Brugian infection. Our data are consistent with a model wherein early resistance to B. malayi is mediated by humoral immune response, with a significant attrition of the incoming infectious larval load. Sterile clearance of the remaining parasite burden appears to require cell-mediated immunity. These data raise the possibility that the identification of molecule(s) recognized by humoral immune mechanisms might help generate prophylactic vaccines. | lld:pubmed |
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| pubmed-article:10684864 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10684864 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10684864 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10684864 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10684864 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:10684864 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:10684864 | pubmed:author | pubmed-author:ShultzL DLD | lld:pubmed |
| pubmed-article:10684864 | pubmed:author | pubmed-author:RajanT VTV | lld:pubmed |
| pubmed-article:10684864 | pubmed:author | pubmed-author:PortePP | lld:pubmed |
| pubmed-article:10684864 | pubmed:author | pubmed-author:PaciorkowskiN... | lld:pubmed |
| pubmed-article:10684864 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10684864 | pubmed:day | 21 | lld:pubmed |
| pubmed-article:10684864 | pubmed:volume | 191 | lld:pubmed |
| pubmed-article:10684864 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10684864 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10684864 | pubmed:pagination | 731-6 | lld:pubmed |
| pubmed-article:10684864 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10684864 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10684864 | pubmed:articleTitle | B1 B lymphocytes play a critical role in host protection against lymphatic filarial parasites. | lld:pubmed |
| pubmed-article:10684864 | pubmed:affiliation | University of Connecticut Health Center, Farmington, Connecticut 06030-3105, USA. | lld:pubmed |
| pubmed-article:10684864 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10684864 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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