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Biology
Published in William Bonnez, Guide to Genital HPV Diseases and Prevention, 2019
Robert C. Rose, Mark H. Stoler
Langerhans cells which are present in the normal epidermis and are professional antigen-presenting cells are usually decreased in number in HPV lesions. During wart regression there is an increase of the density of Langerhans cells and the presence of a mononuclear cell infiltrate, with lymphocytes displaying activation markers. A chemokine and cytokine response is responsible for stimulating this cellular migration and angiogenesis. The molecules involved include tumor necrosis factor (TNF) alpha, monocyte chemotactic protein 1 (MCP-1), chemokine CCL27, vascular endothelial cell growth factor, interferons alpha, beta, and gamma, interleukins 5 and 8, interferon gamma inducible protein (IP-10), retinoic acid, and tumor growth factor (TGF) beta. Although the trigger for wart regression is unknown, viral proteins E5, E6, and E7 are likely responsible for lesion persistence by interacting directly with some of the chemokines and cytokines listed.
Infliximab
Published in John Y. M. Koo, Ethan C. Levin, Argentina Leon, Jashin J. Wu, Alice B. Gottlieb, Moderate to Severe Psoriasis, 2014
Ethan C. Levin, John Y. M. Koo, Alice B. Gottlieb
TNF-α is a proinflammatory cytokine that is elevated in the psoriatic plaques [4] and sera in patients with psoriasis and is a key “driver” cytokine in the pathogenesis of psoriasis. The receptors for TNF-α are expressed on many cell types that are critical to psoriatic inflammation such as lymphocytes, endothelial cells, keratinocytes, and fibroblasts. Depending on the target cell, TNF-α signaling may (i) induce proinflammatory cytokines and chemokines (e.g., interleukin-1 [IL-1], IL-6, nuclear factor kappa B [NF-κB], chemokine ligand 27 [CCL27]), (ii) promote angiogenesis, (iii) induce keratinocyte proliferation, (iv) promote lymphocyte migration to the site of psoriatic inflammation, (v) activate neutrophils and eosinophils, (vi) induce acute phase reactants and tissue remodeling enzymes, or (vii) stimulate fibroblast growth. By blocking TNF-α, infliximab dampens a significant part of the inflammatory cascade that leads to the clinical appearance of psoriasis [3,5,6].
Skin
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Zbigniew W. Wojcinski, Lydia Andrews-Jones, Daher Ibrahim Aibo, Rie Kikkawa, Robert Dunstan
Keratinocytes possess immunologic capabilities through their protein secretion capacities and interaction with T cells as antigen irrelevant signal transducers, antigen/superantigen-specific accessory and presenting cells, and as antigen-specific target cells (Nickoloff and Turka 1993; Nickoloff 2006; Strid et al. 2009). Keratinocytes continuously sample the microbiota colonizing the skin surface through pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), mannose receptors and the NOD-like receptors (Grice and Segre 2011). These receptors recognize pathogen-associated molecular patterns (PAMPs) such as lipopolysacharide and lipoteichoic acids. Upon stimulation, keratinocytes upregulate synthesis and secretion of antimicrobial peptides (AMPs) and signaling peptides including cathelicidins, defensins, and S100 proteins or proteases and protease inhibitors such as LEKT1 involved in skin impermeabilization (Schauber and Gallo 2008; Strid et al. 2009). Keratinocytes also secrete cytokines and chemokines such as IL-1β, IL-6, LI-18, TNF, CCL17, CCL20, CCL27, or IL-15 that are involved in the homing of T cells and neutrophils to the skin, activation of dermal dendritic cells or serve as keratinocyte autocrine factors and T cell and monocyte differentiation factors (Nestle et al. 2009; Strid et al. 2009). Finally, keratinocytes express MHC I and could be induced to express MHC II, although the subsequent induction of immune-competent cells through this expression is still being debated (Salmon et al. 1994). Activated keratinocytes upregulate the expression of adhesion molecules, such as intercellular adhesion molecule 1, which interacts with integrins on the surface of T lymphocytes. Such activation has been demonstrated in various diseases, including psoriasis and hypersensitivity (Salmon et al. 1994). Major skin immune cells and their most prominent functions are listed in Table 21.3.
Correlation analysis between IL-35, IL-36γ, CCL27 and psoriasis vulgaris
Published in Journal of Dermatological Treatment, 2021
Jiao Chen, Jiaxi Du, Yiyang Han, Zhiping Wei
Psoriasis is an immune inflammatory skin disease, which is maintained by a variety of pro-inflammatory pathways, where cytokines and chemokines produced by T cells and epidermal keratinocytes play a major role (18). CCL27 is a skin-specific CC-type chemokine expressed by keratinocytes. It is expressed only in the skin and not in other organs and is expressed constitutively especially in epidermal keratinocytes (19). It can be specifically expressed in skin homing associated antigen positive (CLA+) lymphocytes (20). CCL27 binds to chemokine receptor 10 (CCR10) on skin homing T cells and induces inflammation by promoting the migration of Th1 and Th2 lymphocytes to skin. It is believed that CCL27 plays a key role in T cell-mediated inflammation (21). In psoriatic lesions, suprabasal cells maintain strong CTACK/CCL27 expression due to accelerated proliferation and reduced differentiation (19). It has been reported that TNF-α can upregulate the expression of CTACK/CCL27 and promote the migration of skin lymphocyte-associated antigen positive lymphocytes to skin (19). However, IL-17 plays a key role in downregulating the expression of CCL27 in the late stage of plaque psoriasis. This experiment found that the expression of CCL27 in psoriasis patients was significantly higher than that in normal control group, and the expression was positively correlated with the severity of psoriasis. It is suggest that CCL27 may participate in the pathogenesis of psoriasis as a proinflammatory factor.
Innate lymphoid cells regulate radiation-induced skin damage via CCR10 signaling
Published in International Journal of Radiation Biology, 2020
Yiwen Mao, Rui Tao, Xiaoping Cao, Qin Bao, Dong Wang, Ye Zhao
Radiation-induced skin inflammation is an inevitable complication during radiation therapy. Because of the exposure during radiation therapy, the skin commonly develops inflammation, resulting in thickened, stiff, and discolored tissue with poor wound-healing abilities. ILCs are a group of important immune cells that participate in an early immune response when the skin is stimulated by external factors. The available evidence suggests that alteration in ILCs could contribute to the abnormal immune activation, leading to autoimmunity and chronic inflammatory disorders. Recent studies demonstrated that ILC2s critically promote AD-like inflammation and significantly accumulate in lesioned skin of AD patients (Imai et al. 2013; Kim et al. 2014). ILCs of the skin of healthy people express CCR10, a chemokine receptor involved in the localization of T cells into the homeostatic skin through interaction with CCL27 (Homey et al. 2002; Xia et al. 2014). There is an increasing evidence that CCL27, a ligand of CCR10 secreted by keratinocytes, has a pivotal role in skin inflammation and homeostasis (Xia et al. 2014). Our previous study showed that acute irradiation could induce an increase in the secretion of CCL27 by keratinocytes (Zhang et al. 2017). However, there is few data about the roles of ILCs regulated by CCR10 in radiation dermatitis.
Serum CCL27 predicts the response to Bacillus Calmette-Guerin immunotherapy in non-muscle-invasive bladder cancer
Published in OncoImmunology, 2020
Wenlong Zhong, Bo Wang, Hao Yu, Jianxun Lin, Kun Xia, Weibin Hou, Meihua Yang, Junyu Chen, Meng Yang, Xiaofei Wang, Jian Huang, Tianxin Lin
Despite its long-term use and FDA approval, the mechanisms involved in BCG failure remain poorly understood .16 It has been well established that the Th1/Th2 milieu in TME is consequential for clinical response to BCG therapy.17–19 However, the immunosuppressive mechanisms are multifaceted and heterogeneous for BCG failure. Cumulative evidences support that, in addition to a Th1/Th2 imbalance, several other immune parameters can contribute to BCG failure .20–27 These mechanisms include insufficient immune cell infiltration, 22 the local balance between T lymphocytes and myeloid suppressor cells, 23 adaptive immune resistance,24,25 as well as accumulation of Tregs .26,27 Although CCL27 was usually regarded as a Th2 cytokine,28 we were unable to confirm a link between serum CCL27 and Th2 predisposition in the TME. CCL27 may be non-redundant to Th1/Th2 response in immune regulation during BCG therapy.