Human Thy‐1 induces secretion of matrix metalloproteinase‐9 and CXCL8 from human neutrophils

Saalbach, Anja; Arnhold, Jiirgen; Lessig, Jacqueline; Simon, Jan C.; Anderegg, Ulf

doi:10.1002/eji.200737901

Cited by 20 publications

(17 citation statements)

References 35 publications

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“…In our sample, NBD patients were all under therapy at the time they developed the neurological form and we confirmed the effect of azathioprine on NK depletion in three NDB patients under therapy compared to the other NBD cases (data not shown). Finally, many different chemokines and cytokines are responsible for MMP9 regulation,27 nevertheless, we did not find correlations between any of the investigated soluble factors and MMP9 production.…”

Section: Discussioncontrasting

confidence: 75%

CSF/serum matrix metallopeptidase‐9 ratio discriminates neuro Behçet from multiple sclerosis

Aldinucci

Bonechi

Biagioli

et al. 2018

Ann Clin Transl Neurol

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In neuro Behçet disease with multiple sclerosis‐like features, diagnosis could be challenging. Here, we studied the cerebrospinal fluid and serum inflammatory profile of 11 neuro Behçet and 21 relapsing‐remitting multiple sclerosis patients. Between the soluble factors analyzed (MMP9, TNF α, IL6, CXCL13, CXCL10, CXCL8, IFN γ, IL10, IL17, IL23, and others) we found MMP9 increased in neuro Behçet serum compared to multiple sclerosis and decreased in cerebrospinal fluid. Furthermore, neuro Behçet analysis of circulating natural killer CD56DIM subset suggests their potential involvement in increased MMP9 production. We believe that these findings may have a translational utility in clinical practice.

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Section: Discussioncontrasting

confidence: 75%

CSF/serum matrix metallopeptidase‐9 ratio discriminates neuro Behçet from multiple sclerosis

Aldinucci

Bonechi

Biagioli

et al. 2018

Ann Clin Transl Neurol

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Section: Discussionmentioning

confidence: 99%

“…Moreover, we cannot exclude that interaction of granulocytes or monocytes with Thy-1 might also directly stimulate the secretion of the respective mediators. In fact, the interaction of neutrophils with Thy-1 directly stimulated MMP-9 release [11].In conclusion, Thy-1 mediates the adhesion of granulocytes and monocytes to activated ECs and this interaction plays a pivotal role in the control of the emigration of granulocytes and monocytes from blood into peripheral tissue during inflammation. Consequently, the altered number and composition of extravasated leukocytes affect the inflammatory tissue microenvironment including the chemokine/cytokine and protease pattern.…”

mentioning

confidence: 84%

Section: Introductionmentioning

confidence: 99%

“…Mac-1 expressed on neutrophils and monocytes was identified as a counter receptor for Thy-1 [10]. Furthermore, Thy-1 provides not only the mechanical support for cell adhesion but also triggers neutrophil effector functions, such as the secretion of matrix metalloproteinases (MMP-9) and chemotactic factors (CXCL8) [10,11].Thy-1-deficient mice, originally described by Nosten-Bertrand, are viable [12]. Due to the strong expression of Thy-1 on neuronal cells and T cells (TCs) in mice, previous studies in Thy-1-deficient mice were focused on the investigation of the nervous system and TC functions.…”

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confidence: 99%

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Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

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Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung inflammation, the influx of eosinophils and monocytes was also strongly decreased. These effects were independent of Thy-1 expression on T cells, as shown by the transplantation of WT BM into the Thy-1-deficient mice. In spite of the strong Thy-1 expression on T cells in the chimeric mice, the extravasation of the inflammatory cells in these mice was significantly diminished, compared to control mice. Finally, the altered number and composition of infiltrating leukocytes in Thy-1-deficient mice modified the chemokine/cytokine and protease expression at the site of inflammation. In conclusion, Thy-1 is involved in the control of inflammatory cell recruitment and, thus, also in conditioning the inflammatory microenvironment.Key words: Extravasation . Inflammation . Thy-1 Supporting Information available online IntroductionThe recruitment of inflammatory cells to sites of inflammation plays an important role in the pathogenesis of several inflammatory diseases. Leukocyte adhesion to endothelial cells (ECs) follows a multistep process, including the capture of free leukocytes out of the blood stream, rolling, firm adhesion, and transendothelial diapedesis. The importance of several adhesion molecules in this series of events has been described previously [1]. In ICAM-1-deficient mice, neutrophil recruitment was significantly reduced, but it was not completely blocked in a chemical peritonitis model or in a lipopolysaccharide 645(LPS)-induced airway inflammation model, indicating the involvement of additional adhesion molecules [2,3]. Furthermore, leukocyte recruitment in experimental colitis was not affected by blocking ICAM-1 or MadCAM, whereas the blocking of VCAM-1 resulted in a significant attenuation of colitis [4]. Thus, under specific inflammatory conditions, certain adhesion molecules mediate adhesion and transmigration of leukocytes into the perivascular tissue.Recently, human Thy-1 expressed on ECs was identified as an adhesion molecule mediating the binding of neutrophils and monocytes to activated microvascular ECs [5]. Thy-1 is a highly glycosylated GPI-anchored surface protein and a member of the immunoglobulin superfamily [6,7,8]. In humans, Thy-1 is expressed on ECs at sites of inflammation or in tumours whereas ECs do not express Thy-1 in healthy tissue [5,9]. Thy-1 is also expressed on fibroblasts, neurons, and a su...

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Inflammation, Immunology and Allergy

Steinhoff

2016

Rook's Textbook of Dermatology, Ninth Edition

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Inflammation can be defined as a complex body defence mechanism responding to dangerous endogenous or exogenous stimuli in order to restore body homeostasis. Thus, the skin is continuously challenged to prevent inflammation, and inflammatory skin diseases are very common worldwide. Similarly, allergic reactions (types 1–4) are inflammatory processes created by the body system to respond to ‘danger signals’ of various origins. Very early in phylogenesis, inflammation is associated with the host defence against infectious, allergic or toxic agents, UV radiation, noxious heat and cold, or other injury. Innate and later adaptive immune mechanisms have been established that, uncontrolled, potentially lead to chronic disease or death, as in anaphylactic shock. The body system responds with the induction of various inflammatory pathways such as radical oxygen species, nitric oxide derivatives, complement compounds, adenosine monophosphate, antimicrobial peptides, cytokines, chemokines, prostaglandins, leukotrienes, proteases, neuropeptides and growth factors, just to name a few. This chapter systematically covers the various mechanisms that regulate inflammatory and allergic responses and refers in a translational setting to the diseases that are involved in order better to understand the clinical characteristics of a skin disease, its differential diagnoses and optimal treatment options.

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Human Thy‐1 induces secretion of matrix metalloproteinase‐9 and CXCL8 from human neutrophils

Cited by 20 publications

References 35 publications

CSF/serum matrix metallopeptidase‐9 ratio discriminates neuro Behçet from multiple sclerosis

CSF/serum matrix metallopeptidase‐9 ratio discriminates neuro Behçet from multiple sclerosis

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Inflammation, Immunology and Allergy

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