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Monocyte and lymphocyte membrane markers: Ontogeny and clinical significance
Published in Gabriel Virella, Medical Immunology, 2019
Scott Sugden, Damien Montamat-Sicotte, Karen K. Yam, Joseph Murphy, Bader Yassine Diab, Virginia Litwin
CD226 (DNAM-1) activation results in enhanced NK cell activity (lysis and cytokine production). Receptors for DNAM-1 include two members of the nectin family, the CD155 (poliovirus receptor, PVR) and CD112 (nectin-2), highly expressed on many tumors and normal cells and tissues.
Current and Potential Applications of Pharmacogenetics and Pharmacogenomics
Published in John Y. M. Koo, Ethan C. Levin, Argentina Leon, Jashin J. Wu, Alice B. Gottlieb, Moderate to Severe Psoriasis, 2014
Rishu Gupta, Wilson Liao, John Y. M. Koo, Jashin J. Wu
In addition to polymorphisms in the TNF gene, polymorphisms in the Fc receptor affect the efficacy of TNF inhibitors by enhancing or diminishing affinity for immunoglobulin binding. In a study on rheumatoid arthritis and psoriatic arthritis, Tutuncu et al. found that clinical response to TNF blockers correlated with the Fc-γ receptor type IIIA-158 polymorphism [77]. Furthermore, Genome-Wide Association Study (GWAS) in rheumatoid arthritis have identified additional proposed markers for anti-TNF response including genes encoding transcription factors (AFF3) and cell surface membrane proteins (CD226, CD45/PTPRC) [40,83,84]. Recognition of the polymorphisms may allow practitioners to better optimize the therapeutic approach in order to maximize patient response and limit adverse effects and unnecessary costs.
The Effect of CD226 on the Balance between Inflammatory Monocytes and Small Peritoneal Macrophages in Mouse Ulcerative Colitis
Published in Immunological Investigations, 2022
Juan Li, Feng Zhao, Qi Qin, Liu Yang, Yuan Jiang, Yongli Hou, Yazhen Wang, Wenjing Zhou, Liang Fang, Lihua Chen
CD226 is an immunoglobulin-like glycoprotein, and is involved in a variety of immunological functions (Sherrington et al. 1997). Current research is mainly restricted to the function of CD226 in T cells and NK cells (Dardalhon et al. 2005; Lozano et al. 2012; Sanchez-Correa et al. 2019). CD226 is also expressed on monocytes and macrophages (Reymond et al. 2004; Takenaka et al. 2018; Vo et al. 2016). It was reported iMos selectively expressed high levels of CD226 (Vo et al. 2016). The binding of CD226 and its ligand CD155 prompted monocytes to migrate (Takenaka et al. 2018). In addition, SPMs strongly expressed CD226. CD226 on SPMs contributed to CD4+ T cell costimulation (Reymond et al. 2004). CD226 could also modulate macrophage polarization in post-infarction healing (Li et al. 2020). However, the roles of CD226 in monocyte/macrophage in UC have not been investigated.
Association between CD226 polymorphism and soluble levels in rheumatoid arthritis: Relationship with clinical activity
Published in Immunological Investigations, 2018
Youssef M Mosaad, Ehab ES El-Toraby, Ziyad ME Tawhid, Adel I Abdelsalam, Asmaa F Enin, Amany ME Hasson, Ghada M Shafeek
The Cluster of Differentiation-226 (CD226) gene is located at chromosome 18q22.3 and is composed of seven exons. The CD226 or DNAX Accessory Molecule-1 (DNAM-1) is a 67-kDa type I trans-membrane glycol-protein that belongs to the superfamily of immunoglobulin (Shibuya et al., 1996). CD226 is expressed on immune cells such as natural killer (NK) cells, T lymphocytes and monocytes (Hashemi et al., 2013; Shibuya et al., 2003). There is some evidence regarding the role of CD226 rs763361 polymorphism in autoimmune diseases such as type 1 diabetes (T1D), multiple sclerosis (MS), autoimmune thyroid disease (AITD), Wegener’s granulomatosis (WG), psoriasis, and RA (Douroudis et al., 2010, 2009; Elishmereni et al., 2008; Hafler et al., 2009; Hashemi et al., 2013; Shibuya et al., 1999; Wieczorek et al., 2009; Xiong et al., 2015). It has been proposed that the rs727088 polymorphism in 3`-UTR of CD226 has a functional influence on CD226 transcription levels (Suzuki et al., 2013). The CD226 rs763361 (Gly307Ser) non-synonymous polymorphism could interfere in the phosphorylation of CD226 at 322Tyr and 329Ser residues, and the downstream signal transduction may be modified by these posttranslational modifications (Lofgren et al., 2010; Du et al., 2012; Hashemi et al., 2013; Xu and Jin 2010).
Role of CD226 Rs763361 Polymorphism in Susceptibility to Multiple Autoimmune Diseases
Published in Immunological Investigations, 2020
Linfu Bai, Jinyue Jiang, He Li, Rui Zhang
CD226 gene is of great immunogenetic interest, due to its immunoregulatory effect and potential application in the clinical practice (Kumar et al. 2018). The change of allele at rs763361 (C > T) polymorphism leads to the substitution of glycine with serine (Mattana et al. 2014), but the precise functional effect of rs763361 exchange in the CD226 protein has not yet been elucidated (Wieczorek et al. 2009). A plausible explanation is that the exchange of glycine to serine could interfere in the downstream signaling cascade (Abu El-Ella et al. 2018; Wieczorek et al. 2009), via affecting two neighboring intracytoplasmic phosphorylation sites at 322Tyr and 329Ser residues (Bossini-Castillo et al. 2012; Mattana et al. 2014), which are critical for CD226-mediated signaling. Additionally, the rs763361 polymorphism may modify RNA splicing by disrupting the sequence motif of exon splicing enhancers or silencers, leading to a CD226 isoform with novel or altered function (Alcina et al. 2010; Mattana et al. 2014). As CD226 protein is implicated in differentiation and cytotoxicity of naive T lymphocytes, any interference in the process might contribute to abnormal immune response and subsequent autoimmunity (Mattana et al. 2014). In the experimental autoimmune encephalomyelitis model, anti-CD226 treatment with monoclonal antibody contributed to the delayed onset and reduced severity of encephalomyelitis (Dardalhon et al. 2005; Du et al. 2012). Probably, some drug-like compounds will be developed to target the altered phosphorylation sites or molecular structure of CD226 protein caused by rs763361 polymorphism, which may be an intriguing possibility for treating ADs (Lu 2014).