China 
Africa 
Explore chapters and articles related to this topic
Immune System Imaging
Published in Margarida M. Barroso, Xavier Intes, In Vivo, 2020
Michael J. Hickey, M. Ursula Norman
Leukocyte migration is typically driven by interaction of chemokines with leukocyte-expressed chemokine receptors. In the cortex, chemokine expression is relatively low and uniform with CCL25 and CXCL12 contributing to DN thymocyte accumulation at the SCZ (Plotkin et al., 2003; Bunting et al., 2011; Dzhagalov and Phee, 2012). In the medulla, both the CCR4 ligands (CCL17, CCL22) and the CCR7 ligands (CCL19, CCL21) are highly expressed by medullary DCs, setting up a chemotactic gradient to attract cells expressing the appropriate receptors. After positive selection, thymocytes upregulate CCR4 and CCR7 allowing these cells to migrate into the medulla in response to this chemotactic gradient (Misslitz et al., 2006; Petrie and Zuniga-Pflucker, 2007). 2PM studies show that this migration is blocked by an inhibitor of chemokine receptor signaling. Similarly, positively selected thymocytes deficient in CCR7 showed reduced entry into the medulla following positive selection (Kurobe et al., 2006; Ehrlich et al., 2009), while CCR4 deficiency also reduced the ability of postpositive selection DP and SP CD4 thymocytes to accumulate in the medulla and to interact with medullary DCs (Hu et al., 2015). Together these observations support a role for chemokine-driven migration in these responses.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
Macrophages are key players in the genesis and persistence of COPD. These cells may either mount an inflammatory response directly, or participate in modulating the immune response by promoting healing and repair of damaged airways and parenchyma. Macrophages might acquire different functions as M1- or M2-polarized phenotypes. M1, known as the “classical macrophage,” releases cytokines that induce the expression of pro-inflammatory genes following exposure to inhaled irritants. In contrast, the M2-polarized macrophage participates in repair and healing mechanisms, and immune-regulation. COPD patients may exhibit phenotypic alterations of M1 and M2 populations (Kaku et al. 2014). Such alterations might persist even after smoking cessation and contribute to chronic airway inflammation seen in former smokers (Harada and Basrur 1998; Hodge et al. 2011). In addition, macrophage phagocytic function which is necessary for the resolution of infections and inflammation is impaired in COPD, a process known as “efferocytosis” (Ito et al. 2020; Liu et al. 2020). Efferocytosis refers to the key role macrophages play in the elimination of apoptotic neutrophils and epithelial cells, which if not cleared might lead to secondary inflammatory cascades which contributes to chronic airway inflammation in COPD. Further, Machida et al. (2022) recently demonstrated that lung epithelial cells produce CC motif chemokine ligand 17 (CCL17), a key mediator of cell accumulation in type 2 inflammation that binds to CC chemokine receptor (CCR) 4, upon exposure to cigarette smoke. This CCL17 production is associated with accumulation of alveolar macrophages and development of elastase-induced pulmonary emphysema, possibly through CCL17-induced production of CCL2, a chemoattractant, present in macrophages. These findings may shed new light on the pathogenesis of COPD, and further research is warranted to gain a better understanding of the underlying mechanisms and explore potential therapeutic strategies.