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Immune function of epithelial cells
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Richard S. Blumberg, Wayne Lencer, Arthur Kaser, Jerrold R. Turner
However, in contrast to professional APCs, epithelial cells lack the expression of the classical costimulatory molecules CD80 and CD86 but do express novel members of the B7 family, including inducible costimulatory ligand (ICOS) and programmed death-1 ligand (B7-H1). Further molecules that are relevant for epithelial cell–lymphoid cross talk and are constitutively expressed on epithelial cells are leukocyte function-associated antigen-3 (LFA-3; CD58), E-cadherin, the IL-7 receptor (IL-7R), carcinoembryonic antigen-related adhesion molecule 1 (CEACAM1), and CEACAM5 (CEA), as well as the common γ chain, which is required for signaling through the IL-2R, IL-4R, IL-7R, IL-9R, and IL-15R. CD86 may be expressed on epithelial cells during the inflammation associated with inflammatory bowel disease.
Active Specific Immunization by the Use of Leukemic Dendritic Cell Vaccines
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
Ilse Houtenbos, Gert J. Ossenkoppele, Arjan A. van de Loosdrecht
A second signal termed costimulation is crucial for final T-cell activation. Absence of this second activation signal can lead to T-cell anergy with subsequent tolerance to the presented antigen. A number of molecular interactions contribute to costimulatory signaling. CD28 is the most important costimulatory molecule expressed on naïve T cells and interacts with CD80 and CD86 on APC. Upon activation, T cells will proliferate and differentiate towards effector and memory subtypes. Additionally, T cells upregulate the expression of other costimulatory molecules with either a stimulatory or inhibitory function thereby regulating the immune response.
Polyphenols and Cancer Immunology
Published in Spyridon E. Kintzios, Maria G. Barberaki, Evangelia A. Flampouri, Plants That Fight Cancer, 2019
Curcumin limits the production of inflammatory cytokines by macrophages and enhances T-cell response to IFN-β (Fahey et al. 2007). Moreover, it up-regulates the expression of the co-stimulatory molecule CD86 in DCs and thus improves T-cell activation and conversion to effector T lymphocytes (CTLs), which eradicate tumor cells. Generally, curcumin improves the ‘immune phenotype’ of DCs and reduces the production of anti-inflammatory cytokines by activated T lymphocytes (Milano et al. 2013).
CD44 Drives M1 Macrophage Polarization in Diabetic Retinopathy
Published in Current Eye Research, 2023
Zhujuan Pan, Yaoxin Zhao, Shaobo Zhou, Jing Wang, FeiHong Fan
CD86, also known as B7-2, is an important member of the growing B7 family.28 Since it was initially cloned in the early 1990s, B7-2 was thought to be a factor that could stimulate the growth of decidual stromal cells.29 Interestingly, B7-2 is primarily located on class II human leukocyte antigen + decidual cells and helps to stimulate allogeneic T cells.29 CD86 can interact with CD28 and CD152/cytotoxic T lymphocyte-associated antigen 4 molecules on T cells, which influences T cell survival and response via co-stimulatory and co-inhibitory pathways.30,31 The T cell receptor complex first recognizes the antigen peptide expressed on antigen-presenting cells and binds to MHC, and then the co-stimulatory molecule CD86/CD80 on APC interacts with CD28 on naive T cells to generate stimulatory signals for T cells.32 Diabetes contributed to B cell activation and increased the expression of CD80 and CD86.33 Here, it was discovered that the expression of CD86 was characterized by significant up-regulation in the DR group relative to the control group.
Transdermal delivery of celecoxib and α-linolenic acid from microemulsion-incorporated dissolving microneedles for enhanced osteoarthritis therapy
Published in Journal of Drug Targeting, 2023
Jian Li, Xin Tian, Kang Wang, Yong Jia, Fuguang Ma
In view of synergistic anti-inflammation by combinational celecoxib and α-linolenic acid, the strengthened effects given by microemulsion and microemulsion-incorporated microneedle are validated in this part. As shown in Figure 5(A), celecoxib + α-linolenic acid increased the expression of CD206 of M1-like macrophages compared with the PBS group. Both Cel-MEs and Cel-MEs@MNs can further upregulate the CD206 expression; however, Cel-MEs@MNs did not present a significant difference in macrophage polarisation from Cel-MEs. Likewise, as shown in Figure 5(B), the treatment of celecoxib + α-linolenic acid decreased the CD86 expression of M1-like macrophages. Owing to the potential improvement of cellular uptake, Cel-MEs and Cel-MEs@MNs can also downregulate CD86 expression, which is favourable to anti-inflammatory therapy. As exhibited in Figure 5(C), the celecoxib + α-linolenic acid group can suppress the chondrocytes apoptosis in comparison with the PBS group. Benefiting from the M2 polarisation of macrophages, the apoptosis of chondrocytes in the Cel-MEs and Cel-MEs@MNs group were both significantly inhibited compared with that in the celecoxib + α-linolenic acid group, suggesting the potential of OA therapy through repairing damaged cartilage. Besides, Cel-MEs and Cel-MEs@MNs can both significantly decrease the PGE-2 secretion in comparison to the PBS group (Figure 5D). All the obtained results indicate that microemulsion-incorporated microneedles amplify synergistic anti-inflammation effects by combinational celecoxib and α-linolenic acid, displaying the promising potential in anti-inflammatory-related OA therapy.
Development of a Novel In Vitro Immuno-Competent Model of Dry Eye Disease and Its Use to Evaluate the Efficacy of an Ocular Surface Modulator
Published in Ocular Immunology and Inflammation, 2022
Marisa Meloni, Francesco Carriero, Laura Ceriotti, Stefano Barabino
A multiple endpoint approach has been adopted, including the evaluation of transcriptional activity of specific gene signatures, such as aquaporin 3 (AQP-3) for its crucial role in water channel properties modification in DED, Toll-like receptor 4 (TLR4), which is directly involved in innate immunity response and tumor necrosis factor α (TNF-α) as a biomarker of inflammatory pathway often associated to DED pathology as reported in Table 1. They have been studied at the mRNA level by qRT-PCR in order to have a quantitative approach, while the two biomarkers CD14 and CD86 have been investigated by immuno-staining (immunofluorescence). CD14 is a leucin rich-glycoprotein that functions as co-receptor of cytoplasmatic membrane: it is expressed by undifferentiated THP-1 monocytes and by corneal epithelial cells when interacting with THP-1.18 CD86 is a surface receptor expressed exclusively by dendritic cells or differentiated monocytic cells in APCs19 thus allowing to follow THP-1 dynamic response and to precisely figure out their differentiation. Thus, CD14 and CD86 can be used to discriminate between undifferentiated and differentiated THP-1 monocytes.