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Cell-mediated immunity
Published in Gabriel Virella, Medical Immunology, 2019
José C. Crispín, Gabriel Virella
Finally, CD4 T cells primed in the presence of IL-10 can also become regulatory. These cells, called Tr1 cells, lack FoxP3 and express in their surface CD49b and lymphocyte activation gene (LAG)-3. Tr1 cells can regulate the function of dendritic cells by producing IL-10. Thus, a complex combination of intrinsic and extrinsic factors regulates the immune system to avoid inappropriate and prolonged responses.
The voltage-gated K+ channel Kv1.3 modulates platelet motility and α2β1 integrin-dependent adhesion to collagen
Published in Platelets, 2022
Joy R Wright, Sarah Jones, Sasikumar Parvathy, Leonard K Kaczmarek, Ian Forsythe, Richard W Farndale, Jonathan M Gibbins, Martyn P Mahaut-Smith
Antibodies for analysis of platelet surface antigens included FITC-conjugated rat anti-mouse GPIbα (CD42b, Xia.G5), GPIbβ (CD42c, Xia.C3), GPV (CD42d, Gon.C2) and rat anti-mouse isotype control (P190-1) from Emfret Analytics (Eibelstadt, Germany). Antibodies against integrin chains were FITC-conjugated α2 (CD49b, Ha 1/29), αIIb (CD41, MWReg30), β1 (CD29, Ha2/5), β3 (CD61, 2 C9.G2) and isotype controls from BD Biosciences (Wokingham, UK). Platelet α-granule secretion was measured using anti-P-selectin-FITC (CD62P, Wug.E9) and IgG isotype control, (Emfret Analytics). Horm collagen (type I fibrils from equine tendon) was obtained from Alere (Stockport, Cheshire, UK) and the collagen peptides CRP-XL: crosslinked GCO(GPO)10GCOG-amide, VWF-III: GPC(GPP5)GPRGQOGVMGFO(GPP)5GPC-amide, and GFOGER: GPC(GPP5)GFOGER(GPP5)GPC-amide, were from CambCol Laboratories (Ely, Cambs, UK). Fibrinogen, 3,3ʹ dihexyloxacarbocyanine iodide (DiOC6), prostaglandin E (PGE1), apyrase (type VII), ADP, and hirudin were all purchased from Sigma-Aldrich (Dorset, UK). FM®1-43 lipophilic styryl dye was from Molecular Probes (Life Technologies, Paisley, UK) and Phe-Pro-Arg-chloromethylketone (PPACK) from Hematologic Technologies Incorporated (Vermont, USA). DyLight® 649-conjugated anti-GPIbβ antibody (Emfret Analytics) was used for in vivo thrombus formation experiments.
Using imaging to study inflammatory platelet–leukocyte interactions in vivo
Published in Platelets, 2020
Olivia Susanto, Michael J. Hickey
The optimal approach is to label all endogenous platelets without removing them from the circulation. This can be achieved using intravenously administered, fluorescently conjugated monoclonal antibodies targeting specific platelet surface markers. The most commonly used antibodies target CD41 (GPIIb/αIIb), CD42 (GPIb), and CD49b (α2 integrin) [1,19,30,34–41]. However, there are various reports that administration of either anti-CD41 or anti-CD42 can alter platelet responses and binding function [21,42–44], and that anti-CD41 in particular can induce adverse systemic effects when administered at high doses [43], indicating that careful titration must be employed when using these antibodies. In contrast, anti-CD49b antibody has been reported to label platelets without inducing adverse effects, although possible interference in platelet binding to collagen has been reported [21]. The advantages of using antibodies to label platelets in vivo are that this method is a quick, reliable method to label all platelets in the circulation that can be applied in any mouse strain. This method also allows quantification of platelet aggregate size in vivo [21].
Formation and phenotypic characterization of CD49a, CD49b and CD103 expressing CD8 T cell populations in human metastatic melanoma
Published in OncoImmunology, 2018
Marit M. Melssen, Walter Olson, Nolan A. Wages, Brian J. Capaldo, Ileana S. Mauldin, Adela Mahmutovic, Ciara Hutchison, Cornelis J.M. Melief, Timothy N. Bullock, Victor H. Engelhard, Craig L. Slingluff
RI are mainly expressed on T cells after they infiltrate peripheral tissues, suggesting that they are either lineage markers of a later differentiation stage or induced by molecules in the local tissue environment. Little is known about factors inducing RI expression. TGFβ has been shown to upregulate CD103 expression directly on activated CD8 T cells.22-25 While studies have shown a correlation with the presence of TNFα and TGFβ and CD49a+ T cells in mice,26-28 the direct cause of CD49a induction remains unknown. To our knowledge, factors that induce CD49b have not been identified. Understanding the factors that induce expression of RI is crucial for continued improvements of immune therapies, as it gives perspectives on the role of the TME in retention and dissemination of T cells subsets in the tumor.