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Bronchus-associated lymphoid tissue and immune-mediated respiratory diseases
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Dale T. Umetsu, Bart Lambrecht
Although the respiratory epithelium has been traditionally thought to be primarily a physical barrier and a base for ciliary activity, it is now clear that respiratory epithelial epithelium has a major role in sensing the environment, maintaining homeostasis, and repairing injury. Airway epithelial cells respond to microbial challenge and environmental insults by rapidly producing an array of cytokines and growth factors that initiate innate immunity, prime adaptive immunity, and establish homeostasis. For example, airway epithelial cells respond to PAMPs associated with antigens or microbes that enter the airways, through toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD)-like receptors, and C-type lectin receptors. Signals generated by these receptors or due to direct injury of epithelial cells induce lung epithelial cells to produce cytokines such as interleukin (IL)-1, IL-25, IL-33, thymic stromal lymphopoietin (TSLP), granulocyte-macrophage colony-stimulating factor (GM-CSF), and transforming growth factor (TGF)-β, as well as chemokines (CCL20 [MIP-3α; ligand of CCR6], CCL17 [TARC; ligand of CCR4], and CCL22 [MDC; ligand of CCR4]) and antimicrobial peptides such as defensins. Epithelial cells are also a copious source of endogenous danger signals like adenosine triphosphate (ATP), uric acid, and high mobility group box 1 (HMGB1) that can alert immune cells. Thus, epithelial cells can initiate innate immunity that can later affect adaptive mucosal immunity.
Phagocytic cells and their functions
Published in Gabriel Virella, Medical Immunology, 2019
Gabriel Virella, John W. Sleasman
Macrophages can be separated into three populations: M0, M1, and M2. M0 macrophages are resting cells, able to ingest by phagocytosis or endocytosis, while M1 and M2 are activated macrophage populations. In humans, M1 macrophages, also known as classically activated macrophages, do not endocytose. Two main activation stimuli have been used: LPS and interferon γ (IFNγ). Once activated, they express CD64, and when LPS is added to IFNγ or used by itself, the M1 macrophages also express CD80. M1 macrophages are proinflammatory and express CCL17 and CCL18, but they release different cytokines depending on how they are activated. IFNγ activation induces the release of additional IFNγ, while LPS-activated M1 release very small amounts of IFNγ and predominantly release TNF, IL-1β, RANTES, IL-8, and other proinflammatory cytokines, closer to what is observed when human macrophages are activated via the Fcγ receptors. Activation with IFNγ suppresses the expression of cell recruitment genes activated by LPS, thus suggesting that it can also contribute to the resolution of an inflammatory reaction.
Anisakis
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
Mauricio Afonso Vericimo, Gerlinde Teixeira, Israel Figueiredo, Janaina Ribeiro, Maria Augusta Moulin Fantezia, Sergio Carmona São Clemente
In vitro studies demonstrated that a 24-kDa protein (22U homologous; As22U) derived from A. simplex larva elicits several Th2-related chemokine gene expression, meaning that it may be one of the important allergens for the clinical setting. In order to examine their hypothesis, six intranasal applications of ovalbumin (OVA) or recombinant As22U (rAs22U) and OVA were performed. When compared to the group that only received OVA, the animals challenged with rAs22U associated to OVA presented severe airway inflammation, immune cell recruitment in special, eosinophils, increased levels of IL-4, IL-5, and IL-13 in the Bronchoalveolar lavage fluid (BALF), significantly increased airway hyperresponsiveness, and significantly higher anti-OVA-specific IgE and IgG1. After receiving rAs22U, the GRO-α (CXCL1) gene expression increased immediately while eotaxin (CCL11) and TARC (CCL17) gene expressions increased significantly at 6 h. Thus, rAs22U may be responsible for a Th2/Th17-mediated airway allergic inflammation.124 Using the same experimental protocol, two other Anisakis antigens (Ani s 1 Ani s 9) were tested, eliciting similar results expressing Th2 (IL-4, IL-5, IL-13, e IL-25) and Th17 (IL-6 e IL-17) cytokines because of the intranasal exposure.125
Recovery of systemic hyperinflammation in patients with severe SARS-CoV-2 infection
Published in Biomarkers, 2023
Carolin Langnau, Henrik Janing, Hüseyin Kocaman, Sarah Gekeler, Manina Günter, Álvaro Petersen-Uribe, Philippa Jaeger, Barbara Koch, Klaus-Peter Kreisselmeier, Tatsiana Castor, Dominik Rath, Meinrad Paul Gawaz, Stella E. Autenrieth, Karin Anne Lydia Mueller
Thus, it is tempting to speculate, that especially MIF-positive monocytes are an imprint of severe SARS-CoV-2 infection that may contribute to immunity and re-infection. This conclusion is further substantiated by the fact that a variety of chemokines (e.g., IL-33, CCL17, CXCL1, IL-17A) were elevated months after SARS-CoV-2 infection. IL-33 is a cytokine that induces of T-helper 2 (Th2) cell priming (Komai-Koma et al.2007). CCL17 is chemotactic for T-regulatory cells. CXCL1 serves as chemoattractant for neutrophils (Sawant et al.2016, Metzemaekers et al.2020). IL-17A has been implicated in immune response to infectious pathogens (Ge et al.2020). Thereby, our observations indicate that these elevated cytokine/chemokine levels were also associated with altered and even partly enhanced immune response even after a 3-months recovery phase after COVID-19. However, at present we cannot provide evidence that here observed alterations of plasma chemokines and subsets of circulating monocytes play a role in a sustained protection for re-infection with SARS-CoV-2. We conclude that patients with CVD and acute SARS-CoV-2 infection showed changes regarding their phenotype of monocytes and their chemokine profile after 3-months recovery. Altered monocyte function and increased MIF expression was characteristic for the recovery phase. One can speculate that MIF expression may serve as additional biomarker to identify patients at risk for an altered, possibly prolonged immune response after acute SARS-CoV-2 infection.
CCL22-based peptide vaccines induce anti-cancer immunity by modulating tumor microenvironment
Published in OncoImmunology, 2022
Inés Lecoq, Katharina L. Kopp, Marion Chapellier, Panagiotis Mantas, Evelina Martinenaite, Maria Perez-Penco, Lars Rønn Olsen, Mai-Britt Zocca, Ayako Wakatsuki Pedersen, Mads Hald Andersen
To attract Tregs to the tumor site, tumor cells secrete cytokines and chemokines, such as the C-C motif chemokine ligands (CCLs), CCL28,10 CCL5,11 CCL1,12 and CCL22.3 In particular, CCL22 binds to chemokine receptor 4 (CCR4), which is predominantly expressed on the surface of Tregs, but it is also found on T-helper (th) 2 cells and cutaneous T cells.13 CCL22 accumulation in solid tumors has been shown to lead to Treg infiltration in melanoma, ovarian, prostate, breast carcinomas, and glioblastomas.3,14,15 In contrast, it was shown that tumors that lacked CCL22 expression were not infiltrated by Tregs, regardless of whether they produced other CCR4-binding chemokines, such as CCL17.16 Those findings suggested that the recruitment of Tregs to the TME occurs via the CCL22:CCR4 axis, and it leads to an adverse clinical outcome.16 Furthermore, studies have shown that increased CCL22 expression was associated with the presence of tumor-infiltrating macrophages, an increased presence of Tregs, and a subsequent suppression of host immune responses against cancer cells.13
Biological agents targeting interleukin-13 for atopic dermatitis
Published in Expert Opinion on Biological Therapy, 2022
Andrea Chiricozzi, Niccolò Gori, Martina Maurelli, Paolo Gisondi, Giacomo Caldarola, Clara De Simone, Ketty Peris, Giampiero Girolomoni
Improvements were also detected in terms of both pruritus and the dermatology quality of life index (DLQI) by week 1, with the greatest positive effects observed in the tralokinumab 300 mg Q2W group. At week 12, these beneficial effects reflected improvements in both the physical and mental scoring components, as determined by Short Form-36v2 scoring, and the amelioration of sleep disturbances [59]. Exploratory analyses of biomarkers correlated with clinical responses to tralokinumab revealed greater decreases in serum periostin, CCL17, and IgE concentrations in tralokinumab-treated patients compared to placebo-treated patients, in contrast to serum DPP-4 levels, which increased at the same time point (week 12) [58]. Nevertheless, no clinically meaningful differences in treatment responses were observed in patients with high or low baseline levels of CCL17 and IgE. The safety profile showed that upper respiratory tract infections and headaches were the most common adverse events (AEs) and that most treatment-emergent AEs (TEAEs) were mild or moderate. A low incidence of both viral infections and injection-site reactions was reported. Similarly, conjunctivitis was detected in 2.0% of patients treated with 45 mg tralokinumab, in 5.9% of patients treated with 150 mg tralokinumab, and in 3.9% of patients in the placebo group. Notably, one patient tested positive in an anti-tralokinumab antibody test [58].