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Helper T-Lymphocytes in Cardiovascular Diseases
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Vinay Kumar, Sahil Gupta, Rachel Rosenzweig, Shyam S. Bansal
Pressure overload in rodents, mimicking increased afterload in humans, leads to nonischemic HF and is also associated with increased Th1 polarization72 and infiltration73. Studies have shown that cardiac fibroblasts and CCR2+ macrophages produce CXCL10 and to a lesser extent CXCL9, which attracts CXCR3+ Th1 cells into the failing heart25, suggesting a critical role of the CXCR3-CXCL9/CXCL10 pathway. T-cells in the fibrotic myocardium mainly produce IFNγ, suggesting that Th1 T-cells are the main drivers of cardiac fibrosis in nonischemic HF as well73. Through direct cell-cell contact with cardiac fibroblasts, Th1 T-cells induce TGF-β production and αSMA expression in cardiac fibroblasts to promote their transition into myofibro-blasts73. Thus, both ischemic and nonischemic cardiomyopathies are associated with alterations in the ratio of Th1 to Th2 cells, with chronic HF leading to increased Th1 expression that is proportional to the severity of HF74. An increased ratio of Th1 to Th2 T-cells is also associated with increased production of IFNγ and TNFα in chronic HF75,76.
Immunomodulatory Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
IL-12 is involved in the differentiation of naive T-helper (Th) 0 cells into Th1 cells, and stimulates the production of IFN-γ by plasmacytoid dendritic cells and T cells. IL-12 augments the activity of cytotoxic T cells and enhances B-cell survival. It also induces the production of the chemokine inducible protein-10 (IP-10 or CXCL10), which mediates an antiangiogenic effect. Preclinical models have demonstrated IL-12’s potential as an immunotherapeutic, and this is still being investigated in clinical trials.
West Nile Virus: The Silent Neuro-Invasive Terror
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Vinod Joshi, Annette Angel, Bennet Angel, Neelam Yadav, Jagriti Narang, Surender Yadav
One important feature of our nervous system is that neurons either regenerate or do not regenerate at all. This may indirectly lead to elimination of virus without further multiplication as is the case in WNV infection. During this, the immune system also comes into action (Arjona et al., 2011; Cho and Diamond, 2012; Durrant et al., 2013; Samuel and Diamond, 2006). Interferons are known to play a very important role in virus clearance. It has been studied that T cell and macrophages travel to the brain during WNV infection (Glass et al., 2005, 2006; Shrestha and Diamond, 2004; Shrestha et al., 2006; Wang et al., 2003). On the other hand, CXCL10 (chemokine) is released by neuron cells. T-cell mediated immunity, though, proves to be an effective component during virus clearance but has also shown to cause irreversible damage to the patient (Wang et al., 2003). The regulatory T cells, that is, Treg cells help in controlling viral infection as observed by the presence of high level of Treg cells during asymptomatic infections (Lanteri et al., 2009).
Serum IFNγ–induced protein 10 (IP10/CXCL10): association with asthma exacerbations and severity in children
Published in Journal of Asthma, 2022
Hanan M. Osman, Noussa Ragab El Basha, Ahmed F. Mansour, Mariam Onsy F. Hanna
There is evidence of a quantitative synergistic interaction between allergen sensitization and viral infection in exacerbations (2). Rhinovirus-induced asthma exacerbations in children become more severe as allergen-specific IgE levels increase (31). A high Th1 and IFNγ signature is clinically induced in viral infection, although IFNγ is produced by a variety of immune cells, verifying why it is a challenge to treat exacerbations (3). Virus-specific Th1 cells were found to coordinate with allergen-specific Th2 cells to promote airway inflammation in allergic asthmatic individuals even after the infection resolved and the virus cleared. Both Th1 and Th2 chemoattractants, CXCL10 and CCL22, were strongly induced in infection. Meanwhile, in uninfected asthmatic individuals, higher numbers of virus-specific Th1 cells, but not allergen-specific Th2 cells, were associated with worse lung function (22). It was shown that CXCL10 produced by rhinovirus-infected epithelial cells can direct airway smooth muscle cell chemotaxis and fibroblast migration (32,33), thus it seems plausible that CXCL10 could contribute to the airway remodeling in patients with asthma. It is likely that some of the exacerbation events in our study were triggered by viral infections, although we did not systematically study the cause of the exacerbation. Even though we could not specify the cause of exacerbation, and so could not determine the most important factor in CXCL10 production such as allergic or viral factors, our observations collectively confirm that CXCL10 is an inflammatory biomarker of exacerbations.
ISG56 is involved in CXCL10 expression induced by TLR3 signaling in BEAS-2B bronchial epithelial cells
Published in Experimental Lung Research, 2020
Toshihiro Shiratori, Tadaatsu Imaizumi, Koji Hirono, Shogo Kawaguchi, Tomoh Matsumiya, Kazuhiko Seya, Sadatomo Tasaka
ISG56 functions as an anti-viral molecule through multiple mechanisms.8 For example, it inhibits replication of human papillomavirus by binding to viral E1 helicase,25 blocks replication of hepatitis C virus by interacting with the translation initiation factor eIF3,26 alters the patterns and levels of parainfluenza virus type 5 mRNA and protein synthesis,27 and inhibits viral mRNA translation.28 In the present study, we found that ISG56 knockdown by RNA interference resulted in a decreased in the expression of CXCL10 induced by poly IC, while the expression of another CXC chemokine CXCL1 was not affected. This suggests that ISG56 is selectively involved in the expression of CXCL10. CXCL10 is a member of CXC chemokine family that plays an essential role in host defense against viral infections by stimulating lymphocyte chemotaxis to the infected sites. Therefore, ISG56 may exert anti-viral immune and inflammatory reactions in bronchial epithelial cells, at least partly, by upregulating the expression of CXCL10. CXCL10 also plays diverse roles in the pathogenesis of infectious and inflammatory diseases,10 and serum CXCL10 concentration is correlated with severity of acute respiratory viral infection.29 Dysregulated expression of ISG56 may be associated with inflammatory lung diseases, and this should be investigated in future studies.
Serum Chemokine-release Profiles in AML-patients Might Contribute to Predict the Clinical Course of the Disease
Published in Immunological Investigations, 2020
M. Merle, D. Fischbacher, A. Liepert, C. Grabrucker, T. Kroell, A. Kremser, J. Dreyssig, M. Freudenreich, F. Schuster, A. Borkhardt, D. Kraemer, C.-H. Koehne, H. J. Kolb, C. Schmid, H. M. Schmetzer
Several studies have demonstrated an overexpression of serum-CXCL8 in pts with newly-diagnosed AML and MDS compared to healthy controls (Hantschel et al. 2008; Kittang et al. 2016; Kornblau et al. 2010). Increased levels of CXCL10 were also described in untreated AML/MDS as well as in the course of the disease even after the achievement of complete remission (Olsnes et al. 2009). Furthermore, IL-12-levels were found to be elevated in newly-diagnosed AML compared to healthy controls, where IL-12-release was below detection (Kleiner et al. 2013; Kornblau et al. 2010). In former studies, higher or similar CCL2-levels were seen in untreated AML compared to healthy controls, but lower levels in monocytoid AML (Kornblau et al. 2010; Macanas-Pirard et al. 2017; Mazur et al. 2007). By correlating chemokine-release with cytogenetic risk groups only a decreased CCL2-expression has been observed in cases with intermediate and unfavorable cytogenetic risk (Kornblau et al. 2010).