Elastase is a constituent product of T cells

Bristow, Cynthia L.; Lyford, Lisa K.; Stevens, D P; Flood, Patrick M.

doi:10.1016/s0006-291x(05)81407-x

Cited by 24 publications

(15 citation statements)

References 20 publications

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“…Milk samples were collected from the experimental quarter at 4,8,12,16,25,36,52,64,76, and 316 h postinfusion. All of the peripheral blood and milk samples collected were examined within a few hours after sampling.…”

Section: Methodsmentioning

confidence: 99%

“…Elastase, another enzyme of PMN azurophil granules, present in macrophages and lymphocytes as well, is also involved in leukocyte migration, tissue destruction by digestion of ECM macromolecules, and phagocytosis. It has been reported to be able to cleave such leukocyte antigens as CD4 or CD8 and to modulate leukocyte adhesion by binding to or cleavage of ICAM-1 (8,9,12,15).…”

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confidence: 99%

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Enzymatic Activities of Bovine Peripheral Blood Leukocytes and Milk Polymorphonuclear Neutrophils during Intramammary Inflammation Caused by Lipopolysaccharide

Prin-Mathieu¹,

Roux

Fauré³

et al. 2002

Clin Vaccine Immunol

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Leukocytes are recruited from peripheral blood into milk as part of the inflammatory response to mastitis. However, excessive accumulation of inflammatory cells alters the quality of milk and the proteases produced by polymorphonuclear neutrophils (PMNs) and macrophages may lead to mammary tissue damage. To investigate PMN recruitment and the kinetics of their intracytoplasmic enzymes in inflammation, we generated mastitis in six cows by intramammary infusion of lipopolysaccharide (LPS). Clinical signs of acute mastitis were observed in all of the cows, and normal status was resumed by 316 h. Intracytoplasmic elastase, collagenase, and cathepsin activities were measured within live cells by flow cytometry in peripheral blood leukocytes and milk PMNs before and during the inflammatory process (at 10 time points between 4 and 316 h). The proportion of immature PMNs was appreciated by CD33 surface labeling measured in flow cytometry. Leukopenia was observed in the peripheral blood 4 h postinfusion, concomitant to an increase in somatic cell counts in milk. CD33؉ PMNs were preferentially recruited from the peripheral blood to milk. Enzymatic activities were detected in PMNs, lymphocytes, and monocytes at levels depending on the cell type, sample nature, and time of collection. Milk PMNs had lower enzymatic activities than peripheral blood PMNs. This study showed that milk PMNs recruited during LPS-induced experimental mastitis have an immature phenotype and significantly lower enzymatic activities than peripheral blood PMNs. This suggests that CD33, an adhesion molecule, may be involved in the egress from blood to milk and that the enzymatic contents of PMNs are partly used during this process.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Enzymatic Activities of Bovine Peripheral Blood Leukocytes and Milk Polymorphonuclear Neutrophils during Intramammary Inflammation Caused by Lipopolysaccharide

Prin-Mathieu¹,

Roux

Fauré³

et al. 2002

Clin Vaccine Immunol

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“…Of potential interest to study with references to the malignant cell invasion counterpart are seprase and elastase. While seprase is a membrane bound serine protease with gelatinase activity over expressed in malignant cells and found to associate with MMPs on the cell surface of tumour cells [108], elastase is a serine protease produced also by T cells [109]. …”

Section: Other Matrix-degrading Enzymesmentioning

confidence: 99%

Matrix Metalloproteinases in Cytotoxic Lymphocytes Impact on Tumour Infiltration and Immunomodulation

Edsparr

Basse

Goldfarb

et al. 2010

Cancer Microenvironment

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To efficiently combat solid tumours, endogenously or adoptively transferred cytotoxic T cells and natural killer (NK) cells, need to leave the vasculature, traverse the interstitium and ultimately infiltrate the tumour mass. During this locomotion and migration in the three dimensional environment many obstacles need to be overcome, one of which is the possible impediment of the extracellular matrix. The first and obvious one is the sub-endothelial basement membrane but the infiltrating cells will also meet other, both loose and tight, matrix structures that need to be overridden. Matrix metalloproteinases (MMPs) are believed to be one of the most important endoprotease families, with more than 25 members, which together have function on all known matrix components. This review summarizes what is known on synthesis, expression patterns and regulation of MMPs in cytotoxic lymphocytes and their possible role in the process of tumour infiltration. We also discuss different functions of MMPs as well as the possible use of other lymphocyte proteases for matrix degradation.

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“…17,23,24 Resting peripheral T lymphocytes express a more restricted spectrum of proteases and only upon activation do T cells up-regulate or de novo express MMP-2, MMP-9, cathepsins, members of the PA/plasmin-system, and HLE. [25][26][27] The penetration of T cells and other leukocytes through basement membrane equivalents (matrigel) in vitro is facilitated by active MMP-2 and MMP-9, 26,28 however it remains subject to debate in which tissue compartments and under which conditions matrix proteases contribute to transendothelial migration in vitro and in vivo. [29][30][31][32] Although focalized proteolysis, as established for stromal cells, is an important mechanism supporting cell migration through tissue scaffolds, alternative pathways for bypassing ECM barriers might exist, depending on cell type and ECM environment.…”

Section: Introductionmentioning

confidence: 99%

Amoeboid shape change and contact guidance: T-lymphocyte crawling through fibrillar collagen is independent of matrix remodeling by MMPs and other proteases

Wolf

Mueller

Borgmann

et al. 2003

Blood

391

314

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The passage of leukocytes through basement membranes involves proteolytic degradation of extracellular matrix (ECM) components executed by focalized proteolysis. We have investigated whether the migration of leukocytes through 3-dimensional collagenous tissue scaffolds requires similar ECM breakdown. Human T blasts and SupT1 lymphoma cells expressed mRNA of MMP-9, MT1-MMP, MT4-MMP, cathepsin L, uPA, and uPAR as well as ADAM-9, -10, -11, -15, and -17. Upon long-term migration within 3-dimensional collagen matrices, however, no in situ collagenolysis was obtained by sensitive fluorescein isothiocyanate-collagen fragmentation analysis and confocal fluorescence/backscatter microscopy. Consistent with nonproteolytic migration, T-cell crawling and path generation were not impaired by protease inhibitor cocktail targeting MMPs, serine proteases, cysteine proteases, and cathepsins. Dynamic imaging of cell-ECM interactions showed T-cell migration as an amoebalike process driven by adaptive morphology, crawling along collagen fibrils (contact guidance) and squeezing through pre-existing matrix gaps by vigorous shape change. The concept of nonproteolytic amoeboid migration was confirmed for multicomponent collagen lattices containing hyaluronan and chondroitin sulfate and for other migrating leukocytes including CD8 ؉ T blasts, monocyte-derived dendritic cells, and U937 monocytic cells. Together, amoeboid shape change and contact guidance provide constitutive protease-independent mechanisms for leukocyte trafficking through interstitial tissues that are insensitive toward pharmacologic protease inhibitors. IntroductionThe migration and recirculation of T lymphocytes through the tissues is a multistep process that requires cell adhesion coupled with cellular strategies to overcome physical tissue barriers. 1 The principles of T-cell migration follow the paradigm of "amoeboid" movement established for the single cell state of the lower eucaryote Dictyostelium discoideum. 2,3 Amoeboid movement is a fast lowaffinity migration type driven by a roundish yet flexible cell morphology, dynamic and polarized pseudopod protrusions and retractions, which are independent of focal contact formation and stress fibers. 2 Similar to Dictyostelium, migrating T lymphocytes show an elliptoid polarized shape with a smooth yet dynamically ruffling leading edge, and an additional trailing uropod. 4 This shape generates fast (5-25 m/min) low-affinity gliding across surfaces and through 3-dimensional (3D) collagenous scaffolds 4 driven by a diffuse cortical actin cytoskeleton along the inner leaflet of the plasma membrane devoid of focal contacts at substrate interactions and stress fibers. 5,6 Amoeboid T-cell migration within extracellular matrix (ECM) occurs independently of ␤1 integrin-mediated adhesion both in vitro 6 and in vivo, 7 suggesting differences of the molecular basis between the movement of lymphocytes and other mobile cells, such as fibroblasts and tumor cells. 8,9 After transendothelial migration, T cells and other leukocytes ent...

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Elastase is a constituent product of T cells

Cited by 24 publications

References 20 publications

Enzymatic Activities of Bovine Peripheral Blood Leukocytes and Milk Polymorphonuclear Neutrophils during Intramammary Inflammation Caused by Lipopolysaccharide

Enzymatic Activities of Bovine Peripheral Blood Leukocytes and Milk Polymorphonuclear Neutrophils during Intramammary Inflammation Caused by Lipopolysaccharide

Matrix Metalloproteinases in Cytotoxic Lymphocytes Impact on Tumour Infiltration and Immunomodulation

Amoeboid shape change and contact guidance: T-lymphocyte crawling through fibrillar collagen is independent of matrix remodeling by MMPs and other proteases

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