scholarly journals Very Late Antigen-1 Mediates Corneal Lymphangiogenesis

2011 ◽  
Vol 52 (7) ◽  
pp. 4808 ◽  
Author(s):  
Sammy Grimaldo ◽  
Don Yuen ◽  
Tatiana Ecoiffier ◽  
Lu Chen
Keyword(s):  
Late Antigen ◽  
Corneal Lymphangiogenesis

Leukocytoclastic Vasculitis Associated with HHV6-A/ciHHV6-A and HHV6-B Coinfection in an Immunocompetent Woman

2019 ◽  
Vol 19 (2) ◽  
pp. 221-225 ◽  
Author(s):  
Agata Calvario ◽  
Caterina Foti ◽  
Maria Scarasciulli ◽  
Paolo Romita ◽  
Eva Eliassen ◽  
...  
Keyword(s):  
Transcriptional Activity ◽  
Skin Infection ◽  
Leukocytoclastic Vasculitis ◽  
Human Herpesvirus ◽  
Small Vessel Vasculitis ◽  
Case Description ◽  
Human Herpesvirus 6 ◽  
Late Antigen ◽  
Herpesvirus 6 ◽  
Systemic Symptoms

Background and Objective: Leukocytoclastic vasculitis (LCV) is a small vessel vasculitis that can be limited to the skin but may also affect other organs. Often, its cause is unknown. LCV has previously been reported to occur with the reactivation of human herpesvirus 6 (HHV-6). Here, we report a second instance of HHV-6 reactivation in a 43-year-old woman with idiopathic cutaneous LCV. </P><P> Case Description: In this case, the patient was immunocompetent, and testing revealed that she had inherited chromosomally integrated human herpesvirus 6 variant A (iciHHV6-A) with a parallel skin infection of HHV-6B. The integrated ciHHV-6A strain was found to be transcriptionally active in the blood, while HHV-6B late antigen was detected in a skin biopsy. The patient’s rash was not accompanied by fever nor systemic symptoms and resolved over four weeks without any therapeutic intervention.Conclusion:In light of the transcriptional activity documented in our case, further examination of a possible role for HHV-6 in the etiology of LCV is warranted.

Inflammatory Mediators in Late Antigen-Induced Rhinitis

1985 ◽  
Vol 313 (2) ◽  
pp. 65-70 ◽  
Author(s):  
Robert M. Naclerio ◽  
David Proud ◽  
Alkis G. Togias ◽  
N. Franklin Adkinson ◽  
Deborah A. Meyers ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Late Antigen

How do stem cells find their way home?

Blood ◽  
2005 ◽  
Vol 106 (6) ◽  
pp. 1901-1910 ◽  
Author(s):  
Tsvee Lapidot ◽  
Ayelet Dar ◽  
Orit Kollet
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Lymphocyte Function ◽  
Hematopoietic Stem ◽  
Stem Cell Homing ◽  
Late Antigen ◽  
Multistep Process ◽  
Cell Mobilization ◽  
Membrane Type

AbstractMigration of hematopoietic stem cells through the blood, across the endothelial vasculature to different organs and to their bone marrow (BM) niches, requires active navigation, a process termed homing. Homing is a rapid process and is the first and essential step in clinical stem cell transplantation. Similarly, homing is required for seeding of the fetal BM by hematopoietic progenitors during development. Homing has physiological roles in adult BM homeostasis, which are amplified during stress-induced recruitment of leukocytes from the BM reservoir and during stem cell mobilization, as part of host defense and repair. Homing is thought to be a coordinated, multistep process, which involves signaling by stromal-derived factor 1 (SDF-1) and stem cell factor (SCF), activation of lymphocyte function–associated antigen 1 (LFA-1), very late antigen 4/5 (VLA-4/5) and CD44, cytoskeleton rearrangement, membrane type 1 (MT1)–matrix metalloproteinase (MMP) activation and secretion of MMP2/9. Rolling and firm adhesion of progenitors to endothelial cells in small marrow sinusoids under blood flow is followed by trans-endothelial migration across the physical endothelium/extracellular matrix (ECM) barrier. Stem cells finalize their homing uniquely, by selective access and anchorage to their specialized niches in the extravascular space of the endosteum region and in periarterial sites. This review is focused on mechanisms and key regulators of human stem cell homing to the BM in experimental animal models and clinical transplantation protocols.

scholarly journals Integrin Alpha-9 Mediates Lymphatic Valve Formation in Corneal Lymphangiogenesis

2015 ◽  
Vol 56 (11) ◽  
pp. 6313 ◽  
Author(s):  
Eda Altiok ◽  
Tatiana Ecoiffier ◽  
Roberto Sessa ◽  
Don Yuen ◽  
Sammy Grimaldo ◽  
...  
Keyword(s):  
Lymphatic Valve ◽  
Corneal Lymphangiogenesis ◽  
Valve Formation

scholarly journals Increased levels of VCAM-1 in sera and VLA-4 expression on neutrophils in dermatomyositis with interstitial lung disease

2020 ◽  
Author(s):  
Meiyi Lin ◽  
Xudong Liu ◽  
Chunshu Yang ◽  
Shan Zhao ◽  
Bailing Tian ◽  
...  
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Diffuse Alveolar Damage ◽  
Total Serum ◽  
Enzyme Linked Immunosorbent Assay ◽  
Healthy Controls ◽  
High Resolution Computed Tomography ◽  
Peripheral Blood Neutrophil ◽  
Late Antigen ◽  
And Gender

Abstract Background: Vascular cell adhesion molecule-1(VCAM-1) and its ligand very late antigen (VLA-4) play important roles in many autoimmune diseases. Our study aimed to investigate serum VCAM-1 level and VLA-4 expression on peripheral blood neutrophil surface in patients with dermatomyositis (DM), especially focusing on patients with interstitial lung disease(ILD). Methods: Blood specimens of 30 patients with DM and 30 healthy controls matched for age and gender were recruited. Total serum VCAM-1 level was measured using commercial enzyme-linked immunosorbent assay (ELISA) and the percentages of VLA-4 expression on the surface of neutrophils were analyzed by flow cytometry. We divided patients into subgroups according to whether they had ILD and whether they exhibited diffuse alveolar damage (DAD) via high-resolution computed tomography (HRCT).Results: Serum VCAM-1 levels were increased in DM patients compared with healthy controls (p<0.001). Patients with DM-ILD had higher serum VCAM-1 levels than those with none-ILD (p=0.015). The VCAM-1 levels were significantly increased in the DM-DAD group compared to the none-DAD group (p=0.002). The percentages of VLA-4 expression on neutrophils surface in DM patients were significantly elevated than that in healthy controls (p<0.001). The percentage of VLA-4 expression on neutrophils in DM patients with ILD were higher than none-ILD group(p=0.013). In the patients with ILD, DAD group had higher percentage of VLA-4 expression on neutrophils than none-DAD group (p=0.008).Conclusions: Our findings indicated that serum VCAM-1 level could be used as a potential serological biomarker for DM-ILD.

scholarly journals Cloning and physical mapping of a gene fragment coding for a 64-kilodalton major late antigen of human cytomegalovirus.

1984 ◽  
Vol 81 (15) ◽  
pp. 4965-4969 ◽  
Author(s):  
H. Pande ◽  
S. W. Baak ◽  
A. D. Riggs ◽  
B. R. Clark ◽  
J. E. Shively ◽  
...  
Keyword(s):  
Human Cytomegalovirus ◽  
Physical Mapping ◽  
Gene Fragment ◽  
Late Antigen

scholarly journals Induction of programmed cell death in human hematopoietic cell lines by fibronectin via its interaction with very late antigen 5.

1994 ◽  
Vol 179 (6) ◽  
pp. 1757-1766 ◽  
Author(s):  
H Sugahara ◽  
Y Kanakura ◽  
T Furitsu ◽  
K Ishihara ◽  
K Oritani ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Lines ◽  
Growth Suppression ◽  
Hematopoietic Cell ◽  
Leukemia Cell Line ◽  
Gm Csf ◽  
Late Antigen ◽  
Antigen 5 ◽  
Hematopoietic Cell Lines

Extracellular matrix (ECM) molecules such as fibronectin (FN), collagens, and laminin have important roles in hematopoiesis. However, little is known about the precise mechanisms by which ECM molecules regulate proliferation of human hematopoietic progenitor cells. In this study, we have investigated the effects of ECM molecules, particularly of FN, on the proliferation of a myeloid leukemia cell line, M07E, which proliferates in response to either human granulocyte/macrophage colony-stimulating factor (GM-CSF) or stem cell factor (SCF). The [3H]thymidine incorporation and cell enumeration assays showed that FN strikingly inhibited GM-CSF- or SCF-induced proliferation of M07E cells in a dose-dependent manner, whereas little or no inhibition was induced by collagen types I and IV. The growth suppression of M07E cells was not due to the inhibitory effect of FN on ligand binding or very early events in the signal transduction pathways from the GM-CSF or SCF receptors. DNA content analysis using flow cytometry after staining with propidium iodide revealed that the treatment of M07E cells with FN did not block the entry of the cells into the cell cycle after stimulation with GM-CSF or SCF, whereas the treatment resulted in the appearance of subdiploid peak. Furthermore, FN was found to induce oligonucleosomal DNA fragmentation and chromatin condensation in the cells even in the presence of GM-CSF or SCF, suggesting the involvement of programmed cell death (apoptosis) in the FN-induced growth suppression. The growth suppression or apoptosis induced by FN was rescued by the addition of either anti-FN antibody, anti-very late antigen 5 monoclonal antibody (anti-VLA5 mAb), or GRGDSP peptide, but not by that of anti-VLA4 mAb or GRGESP peptide, suggesting that the FN effects on M07E cells were mediated through VLA5. In addition, the FN-induced apoptosis was detectable in VLA5-positive human hematopoietic cell lines other than M07E cells, but not in any of the VLA5-negative cell lines. These results suggest that FN is capable of inducing apoptosis via its interaction with VLA5, and also raise the possibility that the FN-VLA5 interaction may contribute, at least in part, to negative regulation of hematopoiesis.

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