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| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0018894 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1622501 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1955905 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0333051 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1442792 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0332197 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1413188 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1423842 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0231204 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0475264 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:10899907 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:10899907 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:10899907 | pubmed:dateCreated | 2000-8-10 | lld:pubmed |
| pubmed-article:10899907 | pubmed:abstractText | There is growing evidence that chemokines and their receptors regulate the movement and interaction of antigen-presenting cells such as dendritic cells (DCs) and T cells. We tested the hypothesis that the CC chemokine receptor (CCR)2 and CCR5 and the chemokine macrophage inflammatory protein (MIP)-1alpha, a ligand for CCR5, influence DC migration and localization. We found that deficiency of CCR2 but not CCR5 or MIP-1alpha led to distinct defects in DC biology. Langerhans cell (skin DC) density in CCR2-null mice was normal, and their ability to migrate into the dermis was intact; however, their migration to the draining lymph nodes was markedly impaired. CCR2-null mice had lower numbers of DCs in the spleen, and this was primarily due to a reduction in the CD8alpha(1) T helper cell type 1 (Th1)-inducing subset of DCs. Additionally, there was a block in the Leishmania major infection-induced relocalization of splenic DCs from the marginal zone to the T cell areas. We propose that these DC defects, in conjunction with increased expression of B lymphocyte chemoattractant, a B cell-specific chemokine, may collectively contribute to the striking B cell outgrowth and Th2 cytokine-biased nonhealing phenotype that we observed in CCR2-deficient mice infected with L. major. This disease phenotype in mice with an L. major-resistant genetic background but lacking CCR2 is strikingly reminiscent of that observed typically in mice with an L. major-susceptible genetic background. Thus, CCR2 is an important determinant of not only DC migration and localization but also the development of protective cell-mediated immune responses to L. major. | lld:pubmed |
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| pubmed-article:10899907 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10899907 | pubmed:citationSubset | IM | lld:pubmed |
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