Expansion of circulating NKG2D+ effector memory T-cells and expression of NKG2D-ligand MIC in granulomaous lesions in Wegener's granulomatosis

Capraru, Dorin; Müller, Antje; Csernok, Elena; Gross, Wolfgang L.; Holl‐Ulrich, Konstanze; Northfield, John; Klenerman, Paul; Herlyn, Karen; Holle, Julia; Gottschlich, S.; Voswinkel, Jan; Spies, Thomas A.; Fagin, Ursula; Jabs, Wolfram J.; Lamprecht, Peter

doi:10.1016/j.clim.2007.12.004

Cited by 59 publications

(44 citation statements)

References 20 publications

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“…In this report, sMIC serum levels were also inversely correlated with disease activity (36). Second, in contrast to this "regulatory" phenotype, a "proinflammatory" and cytolytic CD4 þ NKG2D þ T-cell subtype has been described in autoinflammatory diseases such as Wegener's granulomatosis (37,38), rheumatoid arthritis (39), and Crohn's disease (40). In most of these reports, CD4 (29), and in melanoma (42).…”

Section: Nkg2dmentioning

confidence: 61%

Regulation of CD4+NKG2D+ Th1 Cells in Patients with Metastatic Melanoma Treated with Sorafenib: Role of IL-15Rα and NKG2D Triggering

et al. 2014

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Beyond cancer-cell intrinsic factors, the immune status of the host has a prognostic impact on patients with cancer and influences the effects of conventional chemotherapies. Metastatic melanoma is intrinsically immunogenic, thereby facilitating the search for immune biomarkers of clinical responses to cytotoxic agents. Here, we show that a multi-tyrosine kinase inhibitor, sorafenib, upregulates interleukin (IL)-15Ra in vitro and in vivo in patients with melanoma, and in conjunction with natural killer (NK) group 2D (NKG2D) ligands, contributes to the Th1 polarization and accumulation of peripheral CD4 þ NKG2D þ T cells. Hence, the increase of

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Section: Nkg2dmentioning

confidence: 61%

Regulation of CD4+NKG2D+ Th1 Cells in Patients with Metastatic Melanoma Treated with Sorafenib: Role of IL-15Rα and NKG2D Triggering

et al. 2014

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“…ANCA binding to PR3 promotes the release of proinflammatory molecules, leading to endothelial activation and, thereby, increased leukocyte adhesion and tissue infiltration (5). In addition to ANCA-mediated endothelium injury, CD4 T cells likely contribute to GPA pathophysiology (6,7). We (8) demonstrated recently that innate-like T cells that aberrantly express NK cell-activating receptors, such as NKG2D, could exert TCR-independent, IL-15-driven cytotoxicity against vascular ECs.…”

mentioning

confidence: 99%

Tissue-Specific Microvascular Endothelial Cells Show Distinct Capacity To Activate NK Cells: Implications for the Pathophysiology of Granulomatosis with Polyangiitis

Tognarelli

Gayet

Lambert

et al. 2014

The Journal of Immunology

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The relevance of tissue specificity of microvascular endothelial cells (MECs) in the response to inflammatory stimuli and sensitivity to immune cell–mediated injury is not well defined. We hypothesized that such MEC characteristics might shape their interaction with NK cells through the use of different adhesion molecules and NK cell receptor ligands or the release of different soluble factors and render them more or less vulnerable to NK cell injury during autoimmune vasculitis, such as granulomatosis with polyangiitis (GPA). To generate a comprehensive expression profile of human MECs of renal, lung, and dermal tissue origin, we characterized, in detail, their response to inflammatory cytokines and to proteinase 3, a major autoantigen in GPA, and analyzed the effects on NK cell activation. In this study, we show that renal MECs were more susceptible than lung and dermal MECs to the effect of inflammatory signals, showing upregulation of ICAM-1 and VCAM-1 on their surface, as well as release of CCL2, soluble fractalkine, and soluble VCAM-1. Proteinase 3–stimulated renal and lung MECs triggered CD107a degranulation in control NK cell. Notably, NK cells from GPA patients expressed markers of recent in vivo activation (CD69, CD107a), degranulated more efficiently than did control NK cells in the presence of renal MECs, and induced direct killing of renal MECs in vitro. These results suggest that, upon inflammatory conditions in GPA, renal MECs may contribute to the recruitment and activation of NK cells in the target vessel wall, which may participate in the necrotizing vasculitis of the kidney during this disease.

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“…21 Interaction of CD226 with PVR has a role in endothelial transmigration of leukocytes, 22 and anti-CD226 treatment leads to delayed onset and an attenuated disease course in a mouse model of MS. 21 A profound alteration of the T-cell response including Th1 and Th17 responses, natural-killer-likeT-cells anomalously expressing natural killer-receptors, and dysfunctional regulatory T-cells is observed in WG. [23][24][25][26] Thus, similar to T1D, MS and rheumatoid arthritis, in which distinct T-cell alterations are also common, CD226 polymorphisms could predispose to the altered T-cell response in WG.…”

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confidence: 99%

Novel association of the CD226 (DNAM-1) Gly307Ser polymorphism in Wegener's granulomatosis and confirmation for multiple sclerosis in German patients

et al. 2009

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Expansion of circulating NKG2D+ effector memory T-cells and expression of NKG2D-ligand MIC in granulomaous lesions in Wegener's granulomatosis

Cited by 59 publications

References 20 publications

Regulation of CD4+NKG2D+ Th1 Cells in Patients with Metastatic Melanoma Treated with Sorafenib: Role of IL-15Rα and NKG2D Triggering

Regulation of CD4+NKG2D+ Th1 Cells in Patients with Metastatic Melanoma Treated with Sorafenib: Role of IL-15Rα and NKG2D Triggering

Tissue-Specific Microvascular Endothelial Cells Show Distinct Capacity To Activate NK Cells: Implications for the Pathophysiology of Granulomatosis with Polyangiitis

Novel association of the CD226 (DNAM-1) Gly307Ser polymorphism in Wegener's granulomatosis and confirmation for multiple sclerosis in German patients

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