Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi in Psoriasis and Psoriatic Arthritis, 2017
The IL8 receptors include CXCR1 and CXCR2, both GPCRs, and the Duffy antigen receptor for cytokines (DARC), another GPCR-like 7TM protein that is mostly endocytic for CXC and CC chemokines but is not G-protein coupled at the cytosolic end. The pro-angiogenic activity of IL8 occurs predominantly through CXCR2, which is common to other CXC chemokines, but CXCR1 also has some angiogenic action and is unique to IL8 and possibly GCP2 (CXCL6).
Age-associated Ligand-receptor Interactions Imputed from Nasopharyngeal Transcriptomes of COVID-19 Patients
Published in Immunological Investigations, 2022
A recent study of immune cell composition in bronchoalveolar lavage fluid has shown increased expression of pro-inflammatory immune cells expressing more CCR1 and CXCR2 receptors in severe COVID-19 cases (Liao et al. 2020). Indeed, the present study has also shown increased interactions with these receptors in older patients between the NP-M interactions (Figure 1A). Interactions with these receptors were also increased within the microenvironment (M-M) in older patients (Figure 2A). CXCR2 signaling is also a chemokine axis that regulates neutrophil release form the bone marrow (Eash et al. 2010). This is further supported by the increased relative proportions of neutrophils in older patients suggested from computational gene expression deconvolution (Figure 3). Furthermore, CXCL1 and CXCL6 ligands were also shown to be involved in these interactions. CXCL1 secretion has been associated with pro-inflammatory immune cell infiltration (Susek et al. 2018). Formyl peptide receptor 2 (FPR2) interaction with amyloid precursor protein (APP) was also higher in older patients and is implicated in regulating the activation of inflammatory cells (Park et al. 2019). Some notable M-M interactions included SELL receptor interactions with complement factor H (CFH), PODXL2, and CD34, which were decreased relative to the younger patient cohort (Figure 2A). CFH participates in regulation of complement activation (Rodríguez de Córdoba et al. 2004).
Circulating biomarkers of response to immunotherapy and immune-related adverse events
Published in Expert Review of Molecular Diagnostics, 2022
Zachary Garrison, Noah Hornick, Jeffrey Cheng, Rajan P. Kulkarni
CXCL5 is a member of a family of angiogenic chemokines that include CXCL1, CXCL2, CXCL3, CXCL6, CXCL7, and CXCL8. It has long been studied for its role in inflammation and cancer development [80]. More recently, CXCL5 has been identified as a biomarker of TH-17 cell-mediated autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and pemphigus vulgaris [81–83]. This influence on inflammation has also been observed to extend to immune therapy-induced irAEs. A study of advanced melanoma patients on nivolumab identified changes to CXCL5 levels for several types of inflammatory related irAEs including hypophisitis, thyroid dysfunction, adrenal insufficiency, psoriasiform dermatitis, interstitial pneumonia, hepatitis, radiation dermatitis, rheumarthritis, biliary tract disorder, and bursitis, though they did not find a significant trend in their limited sample size [84]. This relationship was also correlated with serum levels of CD163 expressing macrophages. CD163, a receptor found on monocytes [85,86], is linked to CXCL5 via their shared presence on tumor associated macrophages (TAMs). TAM production of CXCL5 [87] is the most rational explanation for the parallel correlation of CXCL5/CD163 and irAEs. CD163+ macrophages are a key component of tumor infiltrating immune cells that produce chemokines associated with cancer development and inflammation [88]. They have already been identified as a marker of autoimmune diseases such as rheumatoid arthritis, pemphigus vulgaris, and bullous pemphigoid [85].
Inhibitory effect of recombinant human CXCL8(3-72)K11R/G31P on atherosclerotic plaques in a mouse model of atherosclerosis
Published in Immunopharmacology and Immunotoxicology, 2019
Yuanhua Qin, Weifeng Mao, Lingmin Pan, Yunliang Sun, Fushun Fan, Ying Zhao, Ying Cui, Xiaoqing Wei, Kazuhiro Kohama, Fang Li, Ying Gao
Atherosclerosis is a pathological process that will induce cardiovascular disease. Recent studies demonstrated that inflammation plays an important role in coronary heart disease, and inflammatory factors are involved in atherosclerosis development [1–8]. Interleukin-8 (IL-8) is an important inflammatory factor and is associated with the development of atherosclerosis [9–12]. High levels of IL-8 are associated with an increased risk of coronary artery disease [13–15]. CXCR1 and CXCR2 are receptors of IL-8, in which CXCR1 also binds to CXCL6/7 but CXCR2 displays higher affinity to IL-8 [16,17]. CXCR2 is a therapeutic target to reduce inflammation [18,19]. CXCL8(3-72)K11R (G31P) is a human IL-8 analog, in which the 11th amino acid (AA) lysine was substituted to arginine, and the 31st AA glycine was substituted to proline [20]. G31P analog has higher affinity to receptors and binds to both CXCR1 and CXCR2 of neutrophils to function in regulating inflammation [21,22]. 0.5 nM G31P can suppress the chemotaxis of neutrophils similar with the levels of 129 nM IL-8/CXCL8 [23]. Some studies reported the roles of CXCL8/G31P on the modulation of inflammation-related angiogenesis and ulcerative colitis [24,25]. However, the role of G31P in atherosclerosis is not defined.