lfa-1 is sufficient in mediating neutrophil emigration in

The Use of Lymphocyte Function–Associated Antigen (Lfa)

The neutrophils from LFA-1 −/− mice have a higher velocity than those from LFA-1 +/+ mice indicating a role for LFA-1 in neutrophil rolling Because LFA-1 does not alter the cell flux (frequency of contact with endothelium) it must be decreasing the velocity by transiently stabilizing the rolling cells A lack of LFA-1 is also reflected in lower adhesion per 100-μm length of mesenteric

LFA

LFA-1 and Mac-1 mediate edema formation and lung injury Cecal ligation and puncture induced significant pulmonary damage indicated by prominent enhancement in lung edema formation () Thus it was found that the lung wet-dry ratio increased by more than 45% in polymicrobial sepsis that is from 4 4 0 1 to 6 4 0 1 (Fig 2 P 0 05 vs sham n = 5)

Lymphocyte function antigen 1 (LFA‐1) mediates early

It was found that 30 min of TNF‐α stimulation increased venular leucocyte adhesion by nearly 10‐fold in LFA‐1‐expressing mice whereas no increase in adhesion was observed in LFA‐1‐deficient animals in response to TNF‐α suggesting that LFA‐1 is a highly important molecule in mediating early TNF‐α‐induced leucocyte adhesion in vivo

Neutrophil Emigration in the Skin Lungs and Peritoneum

Acute emigration of neutrophils requires CD11/CD18 complexes under most circumstances (for review see reference 1) Antibodies against CD11/CD18 inhibit neutrophil emigration during acute inflammation in animals (2 3) Leukocytes from human patients with leukocyte adhesion deficiency type 1 (LAD-1) 1 a disease arising from mutations in the gene for CD18 lack CD11/CD18 complexes

emigration in Mac

LFA-1 Is Sufficient in Mediating Neutrophil Emigration in Mac-1–deficient Mice Huifang Lu * C Wayne Smith * Jerry Perrard ‡ Dan Bullard LiPing Tang i Scott B Shappell Mark L Entman ‡ Arthur L Beaudet ** and Christie M Ballantyne* ‡ *Speros P Martel Laboratory of Leukocyte Biology Department of Pediatrics

Daniel Bullard

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1- deficient mice 1997: 1997: Deficiency of inflammatory cell adhesion molecules protects against atherosclerosis in mice 1997: 1996: Defects in neutrophil function and host defense in IAP-deficient mice 1996: 1996: LFA-1 is sufficient in mediating neutrophil transmigration in Mac-1 knockout mice 1996: 1996: Velocity differences

Huifang Lu

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1 deficient mice J Clin Invest 99:1340-1350 1997 Gopalan PK Smith CW Lu H Berg EL McIntire LB Simon SI Neutrophil CD18-dependent arrest on intercellular adhesion molecule 1 (ICAM-1) in shear flow can be activated through L-selectin J Immunol 158:367-375 1997

Lymphocyte Function

Neutrophil emigration through vascular endothelium is known to be supported by LFA-1 11 but LFA-1 interactions with ligands other than ICAM-1 can support emigration (eg JAM-A56 57 and ICAM-2 58) We have found (unpublished data) that limbal vessels express both JAM-A and ICAM-2 ICAM-2 may contribute to leukocyte infiltration into the cornea

emigration_emigration_emigration__

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1-deficient mice Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2 Using open robust design models to estimate temporary emigration from capture-recapture data Traffic signals for lymphocyte recirculation and leukocyte emigration: the multistep paradigm Traffic

LFA

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1- deficient mice Academic Article Overview Identity Additional Document Info Overview Abstract To better define the specific function of Mac-1 (CD11b) versus LFA-1 (CD11a) and the other CD11 integrins in vivo we have disrupted murine CD11b by targeted homologous recombination in embryonic stem cells and generated mice which are

Lymphocyte Function

Neutrophil emigration through vascular endothelium is known to be supported by LFA-1 11 but LFA-1 interactions with ligands other than ICAM-1 can support emigration (eg JAM-A56 57 and ICAM-2 58) We have found (unpublished data) that limbal vessels express both JAM-A and ICAM-2 ICAM-2 may contribute to leukocyte infiltration into the cornea

Mac

CD18 integrins promote neutrophil recruitment and their engagement activates tyrosine kinases leading to neutrophil activation However the significance of integrin-dependent leukocyte activation in vivo has been difficult to prove Here in a model of thrombohemorrhagic vasculitis the CD18 integrin Mac-1 on neutrophils recognized complement C3 deposited within vessel walls and triggered a

LFA

15 03 1997LFA-1 is sufficient in mediating neutrophil emigration in Mac-1-deficient mice Lu H(1) Smith CW Perrard J Bullard D Tang L Shappell SB Entman ML Beaudet AL Ballantyne CM Author information: (1)Department of Pediatrics Baylor College of Medicine Houston Texas 77030 USA To better define the specific function of Mac-1 (CD11b) versus LFA-1 (CD11a) and the other CD11

Platelet but not endothelial P

In a neutrophil-dependent model of acute postischemic renal failure (APRF) eliminating or blocking P-selectin reduces postischemic neutrophil infiltration and preserves kidney function This study was designed to identify the role of platelet vs endothelial P-selectin in APRF Using wild-type (wt) and P-selectin-deficient (P−/−) mice we generated chimeric mice by bone marrow

be deficient in_be deficient in_be deficient in

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1-deficient mice Inflammatory and Immune Responses are Impaired in Mice Deficient in Intercellular Adhesion Molecule 1 Premature aging in mice deficient in DNA repair and transcription Altered endochondral bone development in matrix metalloproteinase 13-deficient mice Mice Deficient in the α7 Neuronal Nicotinic Acetylcholine

Neutrophil Emigration in the Skin Lungs and Peritoneum

Lu H Smith CW Perrard J Bullard D Tang L Shappell SB Entman ML Beaudet AL Ballantyne CM LFA-1 is sufficient in mediating neutrophil emigration in Mac-1 deficient mice J Clin Invest 1997 99:1340–1350 [PMC free article]

American Journal of Respiratory Cell and Molecular Biology

The process of neutrophil emigration from the systemic circulation has been fairly well defined and occurs in a series of distinct phases during which multiple families of leukocyte and endothelial cell adhesion molecules actively move the neutrophil from the postcapillary venules to the site of inflammation (13 14) The role of each of these families of molecules has not been clearly

Lymphocyte Function

Lymphocyte Function-Associated Antigen--Dependent Inhibition of Corneal Wound Healing200616811 9 Inhibition of neutrophil migration into the cornea extended the healing time by 12 to 24 hours。。Lymphocyte Function-Associated Antigen--Dependent Inhibition Lymphocyte Function-Associated Antigen

JCI

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1-deficient mice Text PDF Abstract To better define the specific function of Mac-1 (CD11b) versus LFA-1 (CD11a) and the other CD11 integrins in vivo we have disrupted murine CD11b by targeted homologous recombination in embryonic stem cells and generated mice which are homozygous for a mutation in CD11b A null mutation was

Neutrophil Adhesion and Migration Relative

Corpus ID: 10969535 Neutrophil Adhesion and Migration Relative Contribution of LFA-1 and Mac-1 to C inproceedings{Ding1999NeutrophilAA title={Neutrophil Adhesion and Migration Relative Contribution of LFA-1 and Mac-1 to C} author={Zhi-Ming Ding and Julia E Babensee and Scott I Simon and Huifang Lu and Jerry L Perrard and Daniel C Bullard and Xiao Yun Dai and Shannon K Bromley

Itgb2

LFA-1 is sufficient in mediating neutrophil emigration in Mac-1-deficient mice J Clin Invest 1997 99:1340-50 pubmed Our results demonstrate that Mac-1 plays a critical role in mediating binding of neutrophils to fibrinogen and neutrophil degranulation but is not necessary for effective neutrophil emigration which is more dependent upon LFA-1 Rosenkranz A Mayadas T Leukocyte

Neutrophil Mechanosignaling Promotes Integrin

Figure 1 Neutrophil recruitment under shear flow is coordinated by selectins chemokines and integrin ligand binding and signaling (A) The sequential steps of neutrophil recruitment under shear flow is initiated by hydrodynamic forces that bring L-selectin and PSGL-1 on the neutrophil surface in contact with P-selectin and E-selectin on the endothelial plasma membrane mediating capture and

Aggravated Lyme Carditis in CD11a−/− and CD11c−/−

These include the absence of the ICAM-3 gene which encodes a ligand for LFA-1 in the mouse a stronger requirement for Mac-1 expression and function in the mediation of neutrophil adhesion to endothelial cells in humans and an apparent increase in the use of alternative non-β2 integrin adhesion pathways in the mouse for mediating neutrophil recruitment (15 20 40) Future studies are

Relative contribution of LFA

To differentiate the unique and overlapping functions of LFA-1 and Mac-1 LFA-1-deficient mice were developed by targeted homologous recombination in embryonic stem cells and neutrophil function was compared in vitro and in vivo with Mac-1-deficient CD18-deficient and wild-type mice LFA-1-deficient mice exhibit leukocytosis but do not develop spontaneous infections in contrast to CD18

Lymphocyte function antigen 1 (LFA‐1) mediates early

It was found that 30 min of TNF‐α stimulation increased venular leucocyte adhesion by nearly 10‐fold in LFA‐1‐expressing mice whereas no increase in adhesion was observed in LFA‐1‐deficient animals in response to TNF‐α suggesting that LFA‐1 is a highly important molecule in mediating early TNF‐α‐induced leucocyte adhesion in vivo

LFA

LFA-1 and Mac-1 mediate edema formation and lung injury Cecal ligation and puncture induced significant pulmonary damage indicated by prominent enhancement in lung edema formation () Thus it was found that the lung wet-dry ratio increased by more than 45% in polymicrobial sepsis that is from 4 4 0 1 to 6 4 0 1 (Fig 2 P 0 05 vs sham n = 5)

LFA

15 03 1997Neutrophil emigration into the peritoneal cavity 16 h after the implantation of fibrinogen-coated disks was not reduced in Mac-1-deficient mice whereas neutrophil adhesion to the fibrinogen-coated disks was reduced by 90% Neutrophils from Mac-1-deficient mice also showed reduced degranulation Our results demonstrate that Mac-1 plays a critical role in mediating binding of

Lymphocyte function antigen‐1 regulates neutrophil

LFA‐1 has been shown to mediate neutrophil adhesion and tissue recruitment (Ding et al 1999 Thorlacius et al 2000) but the role of LFA‐1 in AP is not known Our data show that LFA‐1‐deficient mice exhibited significantly reduced acinar cell necrosis tissue oedema and haemorrhage as well as serum amylase indicating that LFA‐1 plays an important role in mediating organ damage in

Online customer service

Welcome ! If you have any questions or suggestions about our products and services,please feel free to tell us anytime!