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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.
Molecular biology of peritoneal carcinomatosis
Published in Wim P. Ceelen, Edward A. Levine, Intraperitoneal Cancer Therapy, 2015
Riom Kwakman, Nina R. Sluiter, Erienne M.V. de Cuba, Elisabeth (Lisette) A. te Velde
Next to production of chemokines by tumor–stroma cells that directly mediate inflammation, other chemokines are produced to attract certain types of inflammatory cells. Currently, the most investigated lymphocytes are the regulatory T-cells (Tregs). This subset of CD4+CD25+ T-cells exhibits immune modulating properties and is regarded as anti-inflammatory. In the case of PC, Tregs appear to downregulate the antitumor response. CCL22 (stromal-derived factor 1), produced by ovarian carcinoma, might be responsible for the recruitment of Tregs in peritoneal metastases [58]. These Tregs directly inhibit cytotoxic T-cells, which result in decreased levels of antitumorigenic chemokines such as IL-2 and interferon (IFN)-gamma. Tregs produce the chemokines IL-6, IL-10, and TNF-α to promote tumor proliferation [59]. Patients with increased levels of Tregs in their tumor have increased tumor load and decreased survival [58]. Also, when animals with PC are treated with monoclonal antibody to deplete Tregs, IFN-gamma increases, whereas IL-6 decreases, while tumor load decreases in treated animals [59]. The importance of Tregs is increasingly being recognized in PC of different origins [60,61]
Lymphocyte homing and immunology of extranodal lymphoid tissues
Published in Franco Cavalli, Harald Stein, Emanuele Zucca, Extranodal Lymphomas, 2008
Mariagrazia Uguccioni, James J Campbell, Katrin Kuscher, Marshall E Kadin
In CTCL, tumor cells home to the skin because of binding to endothelial cells of dermal capillaries. Circulating CTCL cells expressing CLA roll along endothelial cells expressing E-selectin. CCR4 on MF cells recognize CCL17 or CCL22 on the luminal side of endothelial cells, facilitating binding of LFA-1 on MF cells to ICAM-1 on endothelial cells and subsequent extravasation into the dermis. Ferenczi et al found co-expression of CCR4 and CLA characterized tumor cells in the blood and skin lesions of patients with MF and SS.76 In early MF, tumor cells commonly migrate into the epidermis, a phenomenon known as epidermotropism. Epidermotropism is associated with epidermal keratinocyte secretion of human IFN-inducible protein 10 (CXCL10), which is chemotactic for CD4+ lymphocytes. CXCL10 is confined to basal layer keratinocytes of normal skin but was found to be markedly increased and extended to the superbasal keratinocytes of 17 of 18 CTCL patients.77 CXCL10 expression was not increased in any of 4 patients with B cell lymphoma involving the dermis. Yamaguchi et al reported that CXCR3, the receptor for CXCL10, was especially present in epidermotropic small lymphoma cells of MF.78 MF was distinguished from adult T-cell leukemia/lymphoma (ATLL) by expression of CLA in MF but not ATLL cells.78 Lu found that the CXCR3 was expressed by a subset of tumor lymphocytes in all 25 cases of low-grade MF, with most cells positive in 20 cases.79 In progressed or transformed MF, CXCR3 expression was present in only 5 of 22 cases and in 4 of 5 cases with sequential biopsies, large cell transformation was accompanied by loss of CXCR3. In early MF, tumor cells cluster around Langerhans’ cells in the epidermis, forming Pautrier’s microabscesses which are virtually diagnostic of MF. This process is facilitated by interactions of integrin αEβ7, CCR4, and the T-cell receptor complex on MF cells with E-cadherin, CCL22, and major histocompatibility complex class II antigens, respectively, on Langerhans’ cells. In progressed or transformed MF, CXCR3 is lost, a finding consistent with loss of epidermotropism and downward migration of tumor cells in plaque and tumor stage MF.79
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 assess the ability of each epitope to generate CCL22-specific T cells in vivo, mice were immunized with each CCL22 peptide twice, and one week after the second immunization, CCL22 peptide-specific T-cell responses were evaluated by IFNγ Elispot assay. Two immunogenic CCL22 peptide sequences were identified: (i) for C57Bl/6 mice with predicted affinity for MHC class I H2Db (referred to as CCL2210-19) and (ii) for BALB/c mice predicted to bind to MHC class I H2Ld (referred to as CCL226-14). A significant CCL22-specific immune response was detected in both the spleen (CCL2210-19: Figure 1a-b,=0.0007; CCL226-14: Figure 2a-b,=0.0021) and the lymph nodes (CCL2210-19: Figure 1a,=0.0043; CCL226-14: Figure 2a,<0.0001).
Vitamin D down-regulates the expression of some Th17 cell-related cytokines, key inflammatory chemokines, and chemokine receptors in experimental autoimmune encephalomyelitis
Published in Nutritional Neuroscience, 2019
Abdollah Jafarzadeh, Sayyed Vahab Azizi, Zahra Arabi, Rayhaneh Ahangar-Parvin, Marziyeh Mohammadi-Kordkhayli, Tiziana Larussa, Fariba Khatami, Maryam Nemati
Results from this study also showed that the expression of CCL20, CCL22, and CCR4 in PBS-treated EAE mice was increased compared with healthy controls. It has been demonstrated that both microglia and astrocytes produce chemokine CCL20 and CCL22, which could take a part in the establishment of MS and EAE diseases.67,68 CCL20 could perform a pivotal role in the development of EAE (and MS) during the early phases of the disease. CCR6-deficient mice are highly resistant against the EAE induction by MOG immunization.16 Therefore, the targeting of CCL20 or CCR6 could represent appropriate goals to investigate new treatment strategies for MS in future investigations. Like CCL20, chemokine CCL22 is produced by microglia and astrocytes within the CNS.69,70 In addition to Th2/Treg cells, the CCR4 is expressed by other cells, such as NK, NKT, DCs, and activated T cells.70 It is supposable that the aforementioned cells may also be attracted by CCL22.
Vitamin D and COVID-19: where are we now?
Published in Postgraduate Medicine, 2023
Victoria Contreras-Bolívar, Beatriz García-Fontana, Cristina García-Fontana, Manuel Muñoz-Torres
Green and red arrows indicate activation and inhibition respectively. Proinflammatory cytokines in orange. Anti-inflammatory cytokines in greenish blue. Calcidiol or 25-hydroxyvitamin D: (25(OH)D3). Calcitriol or 1,25-dihydroxyvitamin D3: 1,25(OH)2D3. VDR: Vitamin D receptor, RXR: Retinoid X Receptor. CYP27B1: 25-hydroxyvitamin D-1alpha-hydroxylase. Lt: T Limfocite. Mo: Macrophages. N+: Neutrophil. Th: T Limfocite helper. LT CD4: T Limfocite CD4 + . IFN-α, IFN-γ: Interferon α and γ; IL: Interleukin. TNF-α: Tumor Necrosis Factor-α. TGFβ: Transforming growth factor α and β. CCL22: Chemokine (C-C motif) ligand 2. Ang: angiotensin. ACE2: Angiotensin Converting Enzyme 2.