2011
DOI: 10.3324/haematol.2011.044578
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On the potential involvement of CD11d in co-stimulating the production of interferon-  by natural killer cells upon interaction with neutrophils via intercellular adhesion molecule-3

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Cited by 17 publications
(17 citation statements)
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“…Although the presence of neutrophils is not regarded as a classic feature of IC-induced lupus nephritis, they contribute to the systemic inflammatory response in lupus (49), and we previously described neutrophil extracellular traps in anti-neutrophil cytoplasmic autoantibody-induced small vessel vasculitis glomerulonephritis (50). Interestingly, there is evidence for neutrophils enhancing the survival and proinflammatory properties of slanMo (51)(52)(53).…”
Section: Discussionmentioning
confidence: 89%
“…Although the presence of neutrophils is not regarded as a classic feature of IC-induced lupus nephritis, they contribute to the systemic inflammatory response in lupus (49), and we previously described neutrophil extracellular traps in anti-neutrophil cytoplasmic autoantibody-induced small vessel vasculitis glomerulonephritis (50). Interestingly, there is evidence for neutrophils enhancing the survival and proinflammatory properties of slanMo (51)(52)(53).…”
Section: Discussionmentioning
confidence: 89%
“…In previous observations by other investigators α D β 2 was reported to be expressed on human peripheral blood eosinophils [30], and to be upregulated on human peripheral blood granulocytes [12] and eosinophils [30] in response to stimulation. In a recent report α D was detected on human neutrophils, NK cells, and 6-sulfo- LacNAc + dendritic cells isolated from peripheral blood and cocultured in the presence of cytokines and LPS, although basal expression was apparently not examined [21]. While expression of the protein was not determined, messenger RNA for α D was detected in human peripheral blood monocytes in an earlier report [23].…”
Section: Discussionmentioning
confidence: 94%
“…Several studies have shown that slanDCs interact with neutrophilic granulocytes and natural killer (NK) cells and that this considerably enhances their pro-inflammatory function [20][21][22]. Both contact-dependent (CD18/ICAM-1) and cytokine-mediated (IL-12, IFN-γ) signals are involved in this positive feedback loop.…”
Section: Psoriasismentioning
confidence: 99%