Poliovirus receptor CD155-targeted oncolysis of glioma

Merrill, Melinda K.; Bernhardt, Günter; Sampson, John H.; Wikstrand, Carol J.; Bigner, Darell D.; Gromeier, Matthias

doi:10.1215/s1152851703000577

Cited by 115 publications

(119 citation statements)

References 36 publications

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“…TIGIT/WUCAM Introduction CD155 represents an Ig-like glycoprotein [1] and is the founder of a subfamily of adhesion receptors comprising also the related nectins 1-4. CD155/nectins take part in the complex regulation of cell growth, differentiation and motility [2,3], thereby in part explaining their identification as tumor markers [4][5][6][7]. Current evidence suggests that in contrast to nectins, CD155 acquired immunologically relevant functions.…”

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confidence: 99%

Abundance of follicular helper T cells in Peyer's patches is modulated by CD155

et al. 2009

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The secondary humoral immune response is characterized by plasma B cells secreting isotype-switched and affinity-matured antibodies. The efficient generation of plasma B cells in the GC depends on the presence of follicular helper T (T FH ) cells, a cell type thought to arise from naive CD4-positive T cells by a hitherto unresolved differentiation pathway. Mice deficient for CD155, an adhesion receptor of the immunoglobulin superfamily, are impaired to mount a secondary humoral immune response upon oral administration of antigen, while the primary IgM response is unaffected. Here, we show that mice lacking CD155 harbor significantly reduced numbers of T FH cells in their Peyer's patches. This was paralleled by a decreased frequency of T FH cells in the GC. Moreover, the CD155 ligand CD226, which is involved in T-cell activation, is down-regulated during T FH cell differentiation, resulting in a complete absence of CD226 on those T FH cells residing in the GC. Concurrently, the expression of TIGIT/WUCAM, a newly discovered CD155 ligand, is induced in T FH cells. Thus, these cells replace an activating by a putative inhibitory CD155-binding partner during their differentiation.Key words: CD155 . CD226 . Follicular helper T cells . GC . TIGIT/WUCAM Introduction CD155 represents an Ig-like glycoprotein [1] and is the founder of a subfamily of adhesion receptors comprising also the related nectins 1-4. CD155/nectins take part in the complex regulation of cell growth, differentiation and motility [2,3], thereby in part explaining their identification as tumor markers [4][5][6][7]. Current evidence suggests that in contrast to nectins, CD155 acquired immunologically relevant functions. This apparent, yet not absolute, functional dichotomy in the CD155 family may relate to the observation that CD155 belongs to the category of rapidly evolving genes [8] that may promote the occurrence of new receptor/ligand interactions. In contrast to nectins, CD155 lacks self-adhesion [8]. Instead, CD155 binds to nectin-3 [9], vitronectin [10], CD96 [11,12], CD226 [13] as well as the most recently discovered TIGIT/WUCAM [14,15]. CD155 is broadly expressed among immune cells [16], whereas the expression patterns of the activating receptor CD226 and the potentially inhibitory TIGIT/WUCAM are more restricted. In the T lineage, CD155 is present on T cells of virtually all stages of differentiation, ranging from early thymocytes to the antigen-experienced memory T cells [16]. CD226 is first observed on single positive thymocytes [17] and its subsequent expression is subject to regulation depending on the differentiation path following antigen challenge [18]. Inversely, TIGIT/WUCAM is absent from resting human PBMC and is only expressed upon stimulation [14,15]. Interestingly, immature DC up-regulate CD155 upon stimulation [16], suggesting a role of this receptor in T-cell priming. CD226 was assigned a co-stimulatory capacity [19][20][21] and its interaction with CD155 is pivotal in cytotoxic T/NKdirected lysis of targets such as immature DC...

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Abundance of follicular helper T cells in Peyer's patches is modulated by CD155

et al. 2009

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“…A number of viruses have a natural tropism for tumor cells. This principle is illustrated by the susceptibility of malignant glioma cells to poliovirus, depending on the presence of CD155 on glial neoplasms (14,15). Alternatively, in order to infect the targeted tumor cells, the viral surface binding protein, which has the ability to serve as a receptor, must transform by introducing a single chain antibody or a polypeptide binding ligand: For example, the urokinase receptor (uPAR) is overexpressed in multiple malignancies and serves a role in tumor invasion and angiogenesis (16,17).…”

Section: Specificity Of Ov In Succumbing Tumor Cellsmentioning

confidence: 99%

Advances in the mechanisms of action of cancer-targeting oncolytic viruses (Review)

et al. 2018

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Abstract. Cancer virotherapy mediated by oncolytic viruses (OV), has emerged as a novel and effective strategy in cancer therapeutics. Preclinical models have demonstrated anticancer activity against numerous types of cancer. Currently, a number of recombinant viruses are in late phase clinical trials, many of which have demonstrated promising results regarding the safety and reliability of the treatments, particularly when combined with standard antineoplastic therapies. In addition to molecular-targeted therapeutics, genetic engineering of the viruses allows functional complementation to chemotherapy or radiotherapy agents. Co-administration of chemotherapy or radiotherapy is imperative for an effective treatment regime. Additionally, these approaches may be used in combination with current treatments to assist in cancer management. The near future may reveal whether this renewed interest in oncological virotherapy will result in meaningful therapeutic effects in patients. The aim of the present review was to highlight how the knowledge of oncolytic viral specificity and cytotoxicity has advanced in recent years, with a view to discuss OV in clinical application and the future directions of this field.

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“…However, it is unable to bind nectin-2, but binds CD155 instead (Campadelli-Fiume et al, 2000). CD155 is a poliovirus receptor associated with tumour cell migration and invasion, and has been shown to be up-regulated in human cancers (Merrill et al, 2004;Pende et al, 2005). Genes expressed by BHV-1 are generally named after the coinciding HSV-1 gene, which often have similar activities although there are some functional differences.…”

Section: Bovine Herpesvirus Typementioning

confidence: 99%