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Integrin-Dependent Responses in Human Basophils
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Jane A. Warner, Kirsty Rich, Kirstin Goldring
A second basophil surface marker, CD9, is also reported to act as a receptor for fibronectin (19), and we have found similar results when CD9 is ligated. Clustering of CD9 is sufficient to initiate histamine release in the basophils of some asthmatic patients (see Fig. 1). Ligation of CD9 also modulates the response to a subsequent IgE challenge (see Fig. 1). The basophil responses to CD9 ligation closely resembled the effects of clustering the VLA-4 integrins, and it has been reported that CD9 may associate with VLA-4 on the cell surface (29). These similarities may suggest that CD9 and CD29/CD49d utilize similar signal transduction pathways or that ligation of CD9 causes co-clustering of the VLA-4 integrin and triggers histamine release via this pathway.
Immunology of Scleroderma
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Evidence of antigen driven TCR cell expansion in patients with SSc was determined by the analysis of the TCR gene families. White et al showed an increase in the expression of Vdelta 1 (Vδl) gene on CD3+ T cells and gamma/delta (γ/δ) T cells in lungs.43 A restricted diversity of the TCR junctional regions were identified in Vδ1+ γ/δ T cells isolated from BAL and peripheral blood from patients with SSc compared to controls.4 Absolute numbers and percentages of Vδ1+ T cells were found to be increased in peripheral blood and in skin biopsies.25 Furthermore, these cells were activated and expressed HLA-DR and very late activation antigen (alpha) (CD49d).25 In studies from the active lesions from patients with SSc with less than 18 months disease duration, Sakkas et al found that the Vbeta 13 (νβ13), Vβ14 and νβ21 TCR gene segments were more frequent.45 These results suggests expansion, possibly by antigen-driven selection, of the T cells in SSc patients.
Cellular Trafficking
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
The β1 integrins are also known as the very late antigen (VLA) subfamily because they were first identified on lymphocytes several days after activation.31 At present there are six members, all of which bind to proteins of the extracellular matrix (see Table 6.1). Unlike the other molecules, VLA-4 (CD49d) is found on the majority of unstimulated T lymphocytes, its expression being higher on memory than naive cells.32 It contributes to T-cell adhesion to inflamed endothelium by interacting with VCAM-1 and, as we shall see later, VLA-4 facilitates T-cell infiltration across the BBB in EAE.
Fibronectin modified alginate coating enhances cell targeting and homing to bone marrow in BALB/c mice
Published in Journal of Microencapsulation, 2022
Yogesh Kumar Verma, Gangenahalli Ugraiah Gurudutta
Bone marrow transplantation (BMT) is used for the treatment of many disorders that include radiation injury, immunodeficiencies and leukaemia (Hardy and Ikpeazu 1989). However, shortage of sufficient number of stem cells and premature differentiation in the peripheral vasculature due to growth factors decreases the efficiency of BMT. The engraftment of transplanted stem cells is regulated by the process of migration and homing. Molecules such as, CXCR4, integrins and selectins, mediate rolling, and adhesion of stem cells to endothelium of blood vessels before transendothelium migration to BM (Lapidot et al.2005). Integrins viz. CD49d (VLA4/integrin α4)/CD29 (integrin β1) and CD49e (VLA5/integrin α5)/CD29, play an important role in migration and homing of haematopoietic and progenitor stem cells (Pelayo 2012). Fibronectin, which is a high-molecular weight (∼440kDa) glycoprotein, is found in extracellular matrix and binds to cell membrane-spanning integrin receptors. It also has binding affinity towards extracellular matrix molecules including collagen, fibrin, and heparan sulphate proteoglycans. Fibronectin exists as a dimer, it promotes the process of adhesion and transendothelial migration (TEM) by binding with integrin receptors present on stem cells at BM endothelium (Quesenberry and Becker 1998, Pankov and Yamada 2002).
Singapore Ocular Tuberculosis Immunity Study (SPOTIS): Role of T-lymphocyte Profiling in Patients with Presumed Ocular Tuberculosis
Published in Ocular Immunology and Inflammation, 2021
Paul E. Hutchinson, Ae Ra Kee, Rupesh Agrawal, Nobuyo Yawata, Mayjane Jg Tumulak, John E. Connolly, Soon-Phaik Chee, Jay Siak
For the measurement of the MTB antigen specific CD4 + T cells, the cells were first thawed, then washed and counted, and added to a 96 well plate in RPMI1640/10%FCS (Thermofisher) at a concentration of 2 x 106/200 µl/well. They were then rested overnight at 37°C 5% CO2. The next morning, co-stimulatory antibodies anti-CD28 and -CD49d (eBioscience, USA) were added to a final concentration of 1µg/ml; and Tuberculin PPD 10 µg/ml (Statens Serum Institute, Denmark), recombinant MTB proteins ESAT-6 and CFP-10 10 µg/ml (Lionex, Braunschweig, Germany), or a No Antigen control. The wells were pipetted briefly to mix, and incubated for 1 h at 37°C, 5% CO2. After brefeldin A was added, and the wells were further incubated for another 5 h at 37°C, 5% CO2.
CD38: targeted therapy in multiple myeloma and therapeutic potential for solid cancers
Published in Expert Opinion on Investigational Drugs, 2020
Ying Jiao, Ming Yi, Linping Xu, Qian Chu, Yongxiang Yan, Suxia Luo, Kongming Wu
It has been documented that there is a physical connection between CD38 and CXCR4 on CLL cells and CD38 can significantly synergize with the CXCL12/CXCR4 axis [75]. Accordingly, ERK activation induced by CXCL12-CXCR4 was reduced by treatment with daratumumab in CLL [75]. Some studies in mouse model of myeloma-associated bone loss have demonstrated that CXCL12 in the bone marrow could recruit and activate osteoclast, while CXCL12/CXCR4 axis antagonist significantly restrained osteoblast recruitment [76]. Furthermore, studies have demonstrated that there is a macromolecular complex composed of CD38, integrin CD49d, and the matrix metalloproteinase 9 (MMP9) on CLL cells [77,78]. Convincing evidence demonstrated that CD38 had a physical and quantitative correlation with CD49d on CLL cells and augmented CD49d-mediated cell adhesion [77–79]. The integrin heterodimer CD49d/CD29 on CLL cells and its ligand, VCAM1 promote CLL cells homing to protective niches in the bone marrow and lymph nodes [80,81]. Altogether, these results suggested that CD38 could synergize the effect of CD49d-VCAM1 signals [77–79].