CD44 Antibody Stimulates Adhesion of Peripheral Blood T Cells to Keratinocytes Through the Leukocyte Function–Associated Antigen-1/Intercellular Adhesion Molecule-1 Pathway

Bruynzeel, Ineke; Koopman, Gerrit; Raaij, Liesbeth M.H. van der; Pals, Steven T.; Willemze, Rein

doi:10.1111/1523-1747.ep12472106

Cited by 27 publications

(22 citation statements)

References 28 publications

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“…FAK/SRC-mediated ERK activation is involved in signaling event for stem cell development. Additional receptor proteins for HA include intracellular adhesion molecule-1 (ICAM-1) (Bruynzeel et al, 1993), hyaluronan receptor for endocytosis (HARE) (Pandey and Weigel, 2014), and lymphatic vessel endothelial hyaluronan receptor (LYVE)-1 (Banerji et al, 1999; Lawrance et al, 2016). Clustering of LYVE-1 is essential for HA binding in the lymphatic endothelial cells (Lawrance et al, 2016).…”

Section: Ha Receptors and Signalingmentioning

confidence: 99%

HYAL-2–WWOX–SMAD4 Signaling in Cell Death and Anticancer Response

Hsu

Chiang

Sze

et al. 2016

Front. Cell Dev. Biol.

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Hyaluronidase HYAL-2 is a membrane-anchored protein and also localizes, in part, in the lysosome. Recent study from animal models revealed that both HYAL-1 and HYAL-2 are essential for the metabolism of hyaluronan (HA). Hyal-2 deficiency is associated with chronic thrombotic microangiopathy with hemolytic anemia in mice due to over accumulation of high molecular size HA. HYAL-2 is essential for platelet generation. Membrane HYAL-2 degrades HA bound by co-receptor CD44. Also, in a non-canonical signal pathway, HYAL-2 serves as a receptor for transforming growth factor beta (TGF-β) to signal with downstream tumor suppressors WWOX and SMAD4 to control gene transcription. When SMAD4 responsive element is overly driven by the HYAL-2–WWOX–SMAD4 signaling complex, cell death occurs. When rats are subjected to traumatic brain injury, over accumulation of a HYAL-2–WWOX complex occurs in the nucleus to cause neuronal death. HA induces the signaling of HYAL-2–WWOX–SMAD4 and relocation of the signaling complex to the nucleus. If the signaling complex is overexpressed, bubbling cell death occurs in WWOX-expressing cells. In addition, a small synthetic peptide Zfra (zinc finger-like protein that regulates apoptosis) binds membrane HYAL-2 of non-T/non-B spleen HYAL-2+ CD3− CD19− Z lymphocytes and activates the cells to generate memory anticancer response against many types of cancer cells in vivo. Whether the HYAL-2–WWOX–SMAD4 signaling complex is involved is discussed. In this review and opinion article, we have updated the current knowledge of HA, HYAL-2 and WWOX, HYAL-2–WWOX–SMAD4 signaling, bubbling cell death, and Z cell activation for memory anticancer response.

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Section: Ha Receptors and Signalingmentioning

confidence: 99%

HYAL-2–WWOX–SMAD4 Signaling in Cell Death and Anticancer Response

Hsu

Chiang

Sze

et al. 2016

Front. Cell Dev. Biol.

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“…Engagement of other adhesion receptors may activate CD44 on lympho¬ cytes, thereby enhancing their affinity for hyaluronic acid (23,24). T-cell adhesion is accompanied by the clustering of CD44 molecules on the surface of lymphocytes oriented toward the endothelium (22,25). Within the retroorbital space in GO, CD44 has been localized to connective tissue fibroblasts, vascular endothelium and infiltrating mononuclear cells (26).…”

Section: Comparison Between Go-oecs and Control Oecsmentioning

confidence: 99%

Characterization of adhesion receptors on cultured microvascular endothelial cells derived from the retroorbital connective tissue of patients with Graves' ophthalmopathy

Heufelder

Scriba

1996

European Journal of Endocrinology

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T lymphocytes have been demonstrated recently to play an important role in the pathogenesis and propagation of Graves' ophthalmopathy (GO). Recruitment of T cells to the retroorbital tissue in GO involves the activation of certain adhesion molecules both in the vascular endothelium and in the extravascular connective tissue within the retroorbital space. To characterize the interactions between orbital endothelial cells (OECs) and circulating T cells in vitro, we discussed a two-step immunopurification procedure with bead-immobilized Ulex europaeus I lectin and anti-human endothelial cell antigen (CD31) monoclonal antibody for rapid and reproducible isolation of highly pure microvascular endothelial cell populations from small quantities of retroorbital connective tissue. Endothelial origin of the resulting cell populations was confirmed by positive immunoreactivity for von Willebrand factor. CD31 and thrombomodulin. Under baseline conditions, GO-OECs, but not normal OECs, expressed intercellular adhesion molecule 1 (ICAM-1) and CD44 immunoreactivity but no immunoreactivity for endothelial leukocyte adhesion molecule 1 (ELAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was detected. Exposure of GO-OEC and normal OEC monolayers to interferon gamma, interleukin 1 alpha and tumor necrosis factor alpha resulted in marked up-regulation of immunoreactivity for ICAM-1 and in induction of ELAM-1 and VCAM-1. Blocking experiments using monoclonal antibodies directed against various adhesion molecules demonstrated that interactions between matched activated T lymphocytes and OECs were mediated by integrin-dependent (ICAM-1/leukocyte function-associated antigen 1 (LFA-1): VCAM-1/very late antigen 4 (VLA-4)) and integrin-independent (CD44) pathways, and revealed marked differences when comparing GO-OECs and normal OECs. In conclusion, the availability of OECs from affected retroorbital tissue of patients with GO provides a valuable tool for studying further the mechanisms responsible for orbit-specific lymphocyte recruitment in GO.

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“…They may induce homotypic adhesion of T cells [4,5], and hetero typic adhesion of T cells to dermal fibroblasts [12] or endothelial cells [13]. Moreover, anti-CD44 antibodies may trigger effector functions of T cell clones [ 14] and NK cells [6; Oostendorp, unpubl.…”

Section: Discussionmentioning

confidence: 99%

Adhesion of Human Hematopoietic Progenitor Cells to Bone-Marrow-Derived Stromal Cells Is Enhanced by Antibodies to CD44

Oostendorp¹,

Spitzer²,

Dormer³

1996

Acta Haematol

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It has been suggested that CD44 mediates adhesive interactions between hematopoietic progenitor cells and the stromal microenvironment. Ligands of CD44 include several extracellular matrix components, such as hyaluronic acid and fibronectin. Antibodies against CD44 have been shown to induce homotypic T cell aggregation, and to stimulate T and natural killer cell activity. We hypothesized that CD44 could similarly amplify interactions between blast-colony-forming cells and bone marrow stromal cells (BMSCs). Indeed, we have previously found that the anti-CD44 antibody NKI-P2 enhanced VLA-4-dependent interactions. Here, we studied an additional panel of nineteen anti-CD44 antibodies from the 5th Workshop on Leukocyte Differentiation antigens, to find out whether amplification was associated with a particular CD44 epitope. None of these antibodies showed inhibitory activity, whereas nine significantly increased the number of blast colonies more than 2-fold. Seven of these recognized epitope 1, and two epitope 2. More than 4-fold enhancement was only observed with epitope 1 antibodies: 4.C3 (4.4-fold), 212.3 (6.3-fold), L178 (9.1-fold), and NIH44-1 (9.2-fold). Our data suggest that primarily epitope 1 is associated with enhancement of colony formation. Furthermore, the findings support a role for CD44 as an amplifier in progenitor-BMSC interactions.

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CD44 Antibody Stimulates Adhesion of Peripheral Blood T Cells to Keratinocytes Through the Leukocyte Function–Associated Antigen-1/Intercellular Adhesion Molecule-1 Pathway

Cited by 27 publications

References 28 publications

HYAL-2–WWOX–SMAD4 Signaling in Cell Death and Anticancer Response

HYAL-2–WWOX–SMAD4 Signaling in Cell Death and Anticancer Response

Characterization of adhesion receptors on cultured microvascular endothelial cells derived from the retroorbital connective tissue of patients with Graves' ophthalmopathy

Adhesion of Human Hematopoietic Progenitor Cells to Bone-Marrow-Derived Stromal Cells Is Enhanced by Antibodies to CD44

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