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Application of Stem Cell and Exosome-Based Therapy in COVID-19
Published in Debmalya Barh, Kenneth Lundstrom, COVID-19, 2022
Suleyman Gokhan Kara, Ayla Eker Sariboyaci
MSC-mediated immunomodulation is regulated through cell-to-cell contact and various soluble factors. It has been found that the stimulation of the surface receptors of MSCs by RNA viruses leads to immunomodulation. The immunomodulation of MSCs is mediated by TLRs (mainly TLR3 and TLR4) present on the surface of MSCs [10]. RNA viruses activate these TLRs, which leads to secretion of chemokines (MIP-1α, MIP-1β, CXCL9, CXCL10, CXCL11, and RANTES), and these initiate the anti-inflammatory immune response [10]. This response can be beneficial in a cytokine storm, where a hyper-proinflammatory response is triggered by SARS-CoV-2 in COVID-19 patients.
Anti-infectious innate and adaptive immune responses
Published in Gabriel Virella, Medical Immunology, 2019
Carl Atkinson, Gabriel Virella
Interleukin-8 (neutrophil-activating factor) is the most important of the CXC chemokines. It is released by T lymphocytes and monocytes stimulated with TNF or IL-1. It functions as a chemotactic and activating factor for granulocytes, the cell population with the highest level of IL-8 receptor expression. IL-8 recruits granulocytes to areas of inflammation and increases their phagocytic and pro-inflammatory abilities. It has also been demonstrated to be chemotactic for T lymphocytes. In addition to IL-8, the CXC chemokines include the previously mentioned interferon-γ–inducible chemokines (CXCL9, CXCL10, and CXCL11).
Viral infections in lung transplantation
Published in Wickii T. Vigneswaran, Edward R. Garrity, John A. Odell, LUNG Transplantation, 2016
Lara Danziger-Isakov, Erik Verschuuren, Oriol Manuel
The potential immunologic mechanisms underlying this epidemiologic association are currently being investigated. Weigt and colleagues reported that increased concentrations of the chemokine receptor CXCR3 ligands CXCL10 and CXCL11 in BAL fluid during CARV infection were associated with greater declines in FEV1 at 6 months after infection.22 With the improvement in molecular diagnostics for respiratory virus,23 increased surveillance, and increased insight into the potential mechanisms of inflammatory injury with CARV, the association between CARV and BOS can be further delineated and measures for novel treatment strategies developed.
Current concepts in the pathogenesis of periodontitis: from symbiosis to dysbiosis
Published in Journal of Oral Microbiology, 2023
Ali A. Abdulkareem, Firas B. Al-Taweel, Ali J.B. Al-Sharqi, Sarhang S. Gul, Aram Sha, Iain L.C. Chapple
The benefits for the whole microbial community are supported by another immune subversion mechanism induced by P. gingivalis, localized chemokine paralysis [140]. The suppression of chemotactic IL-8 is induced through the action of serine phosphatase B (SerB) whereby P. gingivalis dephosphorylates S536 residue of p65 sub unit of nuclear factor kappa B, suppressing transcription of CXCXL8 (IL-8) [168]. In addition, the chemokine suppression of CXCL9, CXCL10 and CXCL11 is mediated through the invading P. gingivalis blocking the signal transducer and activator of transcription 1 (STAT1)-interferon regulatory factor 1 (IRF1) pathway in epithelial cells and neutrophils. This promotes T cell imbalance by suppression of TH1-associated activities, including downregulating IL-12 and activation of TH17-associated activities including upregulation of pro-inflammatory IL-6 and IL-23 cytokines, thereby enhancing the inflammatory response and bone loss [169] (Figure 8).
Lacticaseibacillus paracasei sh2020 induced antitumor immunity and synergized with anti-programmed cell death 1 to reduce tumor burden in mice
Published in Gut Microbes, 2022
Shi-Long Zhang, Bing Han, Yu-Qin Mao, Zheng-Yan Zhang, Zhan-Ming Li, Chao-Yue Kong, You Wu, Guo-Qiang Chen, Li-Shun Wang
To explore the potential mechanisms of L. paracasei sh2020, we performed RNA-seq analysis of tumor tissues harvested from the mice treated with vehicle, or L. paracasei sh2020. First, GSEA analysis identified high-level categories, such as regulation of T cell mediated immunity, leukocyte migration, positive regulation of adaptive immune response, were enriched in the L. paracasei sh2020-treated tumors (Figure 5a). Notably, this group promoted the expression of T cell chemoattractant chemokines (Figure 5b-c), such as CXCL9, CXCL10, and CXCL11, previously described to be involved in modulating the tumor immune environment.25 Next, the RNA-seq data were then analyzed to estimate the tumor-infiltrating immune cell. We also found that there was a greater proportion of CD8+ T cells in the L. paracasei sh2020-treated tumors (Figure S4). These results suggested that L. paracasei sh2020 might elicit chemokines expression in the tumors, which ultimately promoted CD8+ T cell infiltration into the tumor beds.
A Novel Class of On-Treatment Cancer Immunotherapy Biomarker: Trough Levels of Antibody Therapeutics in Peripheral Blood
Published in Immunological Investigations, 2022
Yoshinobu Koguchi, William L. Redmond
In our previous work, we identified baseline, but not on-treatment, CXCL11 as a predictive biomarker that was negatively associated with clinical outcome in patients with advanced melanoma treated with ipilimumab but not in patients treated with a gp100 vaccine (Koguchi et al. 2015). We hypothesized that baseline CXCL11 reflects pre-treatment conditions affecting clinical outcome and trough levels of ipilimumab, but independently. To address this hypothesis, we conducted a multivariate analysis including trough levels of ipilimumab and CXCL11 along with other demographic information as confounding factors to assess the association of both factors with OS. When we used trough levels of ipilimumab as a categorical valuable (below or above median), CXCL11 lost its association with clinical outcome. On the other hand, when we used trough levels of ipilimumab as a continuous valuable, then trough levels of ipilimumab, but not CXCL11, lost association with clinical outcome (Koguchi et al. 2021). These results suggested that baseline conditions are likely responsible for elevated CXCL11 levels and lower trough levels of ipilimumab.