2005
DOI: 10.1073/pnas.0408288102
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Glycolipid presentation to natural killer T cells differs in an organ-dependent fashion

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Cited by 113 publications
(91 citation statements)
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References 43 publications
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“…Viruses cDC requirement for LCMV, 35 HSV-1, 36 VSV, 37 influenza, 38 CTL response cDC independence of anti-VSV B and CD4 T-cell response 36,39 Bacteria cDC requirement for anti-Listeria CTL response 11,40 cDC requirement for efficient Mycobacterium tuberculosis CD4 T-cell response 41 cDC requirement for anti-Salmonella response 42,43 cDC independence of UPEC clearance 44 Parasites cDC requirement for anti-Plasmodium 11 and anti-Leishmania response 45,46 Prions cDC requirement for intestinal Scrapie agent neuroinvasion 47 Miscellaneous Tolerance cDC role in Ig complex-mediated priming and tolerization 48,49 cDC independence of peripheral CD4 T-cell tolerization 50 NK responses cDC requirement for NK cell activation by IL-15 trans-presentation 25 NKT responses cDC requirement for glycolipid presentation 51,52 CTL responses cDC requirement for efficient CTL memory generation 27 Respiratory tract cDC requirement for asthma and experimental allergic rhinitis 18,53 Tumor studies cDC requirement for antitumor immunity 52 DC functions by conditional cell ablation A Sapoznikov and S Jung subpopulations and generally provided by non-hematopoietic cells, including stromal and follicular dendritic cells; 58 and (2) the chemokine macrophage migration inhibitory factor (MIF) that controls mature B-and tumor cell survival through triggering of the CD74-CD44 receptor complex. [59][60][61] 70 on pDC.…”
Section: Pathogen Defensementioning
confidence: 99%
“…Viruses cDC requirement for LCMV, 35 HSV-1, 36 VSV, 37 influenza, 38 CTL response cDC independence of anti-VSV B and CD4 T-cell response 36,39 Bacteria cDC requirement for anti-Listeria CTL response 11,40 cDC requirement for efficient Mycobacterium tuberculosis CD4 T-cell response 41 cDC requirement for anti-Salmonella response 42,43 cDC independence of UPEC clearance 44 Parasites cDC requirement for anti-Plasmodium 11 and anti-Leishmania response 45,46 Prions cDC requirement for intestinal Scrapie agent neuroinvasion 47 Miscellaneous Tolerance cDC role in Ig complex-mediated priming and tolerization 48,49 cDC independence of peripheral CD4 T-cell tolerization 50 NK responses cDC requirement for NK cell activation by IL-15 trans-presentation 25 NKT responses cDC requirement for glycolipid presentation 51,52 CTL responses cDC requirement for efficient CTL memory generation 27 Respiratory tract cDC requirement for asthma and experimental allergic rhinitis 18,53 Tumor studies cDC requirement for antitumor immunity 52 DC functions by conditional cell ablation A Sapoznikov and S Jung subpopulations and generally provided by non-hematopoietic cells, including stromal and follicular dendritic cells; 58 and (2) the chemokine macrophage migration inhibitory factor (MIF) that controls mature B-and tumor cell survival through triggering of the CD74-CD44 receptor complex. [59][60][61] 70 on pDC.…”
Section: Pathogen Defensementioning
confidence: 99%
“…In their studies, they used a C-glycosidic form of ␣-GalCer in analyses of the adjuvant properties of ␣-GalCer. It was found that the C-glycoside induced more of a Th1 (i.e., IFN-␥) response, was longer lasting, and was actually a better adjuvant than the parental compound itself in murine models of malaria and metastatic melanoma (53)(54)(55)(56)(57). Furthermore, ␣-GalCer administration has been shown to be mostly protective activity against viruses (58 -61), bacteria (62)(63)(64)(65)(66)(67), and other pathogens (68,69).…”
Section: ␣-Galactosylceramide (␣-Galcer) and ␣-Galcer Analogsmentioning
confidence: 99%
“…Although special roles for tissue-specific APCs in activating iNKT cells have recently been described, in theory any CD1d ϩ cell is capable of eliciting some type of iNKT cell response (27). To address the possibility that the observed Lck-CD1d Tg ϩ iNKT cell phenotype is due to the selective absence of CD1d on some cell types, we repeated the in vivo ␣-GalCer stimulation assays in both Lck-CD1d TgCD1°and Lck-CD1d TgCD1 ϩ mice, the latter of which maintain the endogenous CD1d expression program.…”
Section: Inefficient Ag Presentation Cannot Account For the Hyporespomentioning
confidence: 99%
“…The mechanism(s) regulating iNKT function is unclear. Functional differences in iNKT cells in various disease models may be mediated by the quality of the stimulating signal, which may be attributable to differential TCR/ligand interactions (25,26) and selective presentation of Ag by different CD1d-expressing cell types (27). Activation of phenotypically and/or anatomically distinct subsets of iNKT cells may also account for differences in iNKT function.…”
mentioning
confidence: 99%