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Immunomodulating Agents in Gastrointestinal Disease
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Samir A. Shah, Athos Bousvaros, A. Christopher Stevens
Monoclonal therapies that block leukocyte adhesion have been suggested for the treatment of intestinal diseases. CD18 is a molecule in the integrin family that forms heterodimers with CD11 isotype molecules. CD18/CD11 is a leukocyte adhesion molecule expressed on vascular endothelium and the basolateral surfaces of epithelial cells. Anti-CD18 antibody blocks the adhesion of leukocytes to these sites, preventing extravasation of leukocytes into tissues and across epithelial barriers [204,205]. Pretreatment with anti-CD 18 has been effective in preventing the colonic inflammation in the TNBS rabbit model of colitis [206]; however, it remains untested in humans. Another integrin, very late antigen (VLA4), functions in the adhesion of leukocytes and has been a target of monoclonal antibody therapy in the treatment of the cotton-topped tamarin animal model of ulcerative colitis [207].
The Role of Neutrophils and Reactive Oxygen Metabolites in Reperfusion Injury
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Barbara J. Zimmerman, D. Neil Granger
The neutrophil membrane glycoprotein CD11/CD18 has been shown to play an important role in mediating neutrophil adhesion to microvascular endothelium. Monoclonal antibodies directed against the functional epitope of CD11/CD18 have been shown to inhibit the chemotaxis, aggregation, and adherence to endothelial monolayers of neutrophils.28 These monoclonal antibodies (MAb 60.3, IB4) have been used to examine the role of leukocyte adhesion in the microvascular and parenchymal cell injury induced by reperfusion of ischemic tissues. It has been demonstrated that administration of MAb 60.3 is as effective as neutropenia in attenuating the reperfusion-induced increase in intestinal microvascular permeability.28 In addition, Kurtel et al. have demonstrated that pretreatment with IB4 prevents the rise in myeloperoxidase levels observed in all layers of the bowel wall and mesentery following ischemia/reperfusion.29 These observations indicate that reperfusion-induced leukocyte-endothelial cell interactions are mediated by the leukocyte adhesion glycoprotein complex CD11/CD 18.
Diagnosis of immune deficiency diseases
Published in Gabriel Virella, Medical Immunology, 2019
John W. Sleasman, Gabriel Virella
Phagocytic cell function tests were discussed in detail in Chapter 13. Testing for defects in phagocytic numbers and function involves three common tests for different types of phagocyte deficiency. A complete blood count with differential tests for congenital neutropenia as well secondary causes of neutropenia due to drug toxicity, infection, or malignancy. This confirmatory test for neutropenia requires bone marrow aspirate and biopsy. Leukocyte adhesion deficiency, types I, II, or III, can be made from cytometry. Loss of expression of CD11/18 markers on neutrophils and monocytes is used to diagnosis type I leukocyte adhesion deficiency, the most common subtype. In contrast to congenital neutropenia, these patients have persistently elevated white cell counts. Flow cytometry–based assays that measure the neutrophil oxidative burst by fluorescence changes in cells stimulated with phorbol myristate acetate (PMA) are widely used for the diagnosis of chronic granulomatous disease (CGD).
Addition of camrelizumab to docetaxel, cisplatin, and radiation therapy in patients with locally advanced esophageal squamous cell carcinoma: a phase 1b study
Published in OncoImmunology, 2021
Wencheng Zhang, Cihui Yan, Tian Zhang, Xi Chen, Jie Dong, Jingjing Zhao, Dong Han, Jun Wang, Gang Zhao, Fuliang Cao, Dejun Zhou, Hongjing Jiang, Peng Tang, Lujun Zhao, Zhiyong Yuan, Quanren Wang, Ping Wang, Qingsong Pang
We applied multi-color immunofluorescence to dynamically monitor the tumor immune microenvironment (Figure 3a and b). Of the 18 patients who were assessed for baseline PD-L1 expression, 8 (44%) had PD-L1-positive tumors using a cutoff value of 7.613%. High baseline tumor PD-L1 expression tended to be associated with longer OS (Figure 3c). Radiation could convert the tumor into an in situ vaccine, promoting cross-presentation of tumor-derived antigens by dendritic cells to T cells.23 And macrophages programmed by radiotherapy might exhibit double activity to anti-tumor effect.24 Both dendritic cells and macrophages partially contributed to the expression of PD-L1 except tumor cells. As a result, we identified dendritic cells and macrophages in the tumor microenvironment before and during treatment. We found high baseline levels of tumor CD11+ dendritic cells were related to improved OS (Figure 3d). None of immune-cell subsets during treatment was associated with patient survival.
Combination checkpoint therapy with anti-PD-1 and anti-BTLA results in a synergistic therapeutic effect against murine glioblastoma
Published in OncoImmunology, 2021
John Choi, Ravi Medikonda, Laura Saleh, Timothy Kim, Ayush Pant, Siddhartha Srivastava, Young-Hoon Kim, Christina Jackson, Luqing Tong, Denis Routkevitch, Christopher Jackson, Dimitrios Mathios, Tianna Zhao, Hyerim Cho, Henry Brem, Michael Lim
Next, expression of BTLA and its ligand HVEM was studied in the glioma setting on various tumor-infiltrating immune cell populations including CD45+ CD3 + T cells, CD45+ CD11b+ cells (commonly denoting macrophages), CD45+ CD11 c+ cells (commonly denoting macrophages and dendritic cells) and CD45+ CD19 + B cells (Supplemental Figure S1). There was significantly lower HVEM expression on CD3+ TILs compared to tumor-infiltrating CD11b+ cells (P < .0001), CD11 c+ cells (P < .0001), or CD19 + B cells (P < .0001) (Supplemental Figure S1b). There was significantly lower BTLA expression on CD11 c+ cells compared to CD3 + T cells (P = .0405) and tumor-infiltrating CD11b+ cells (P = .0062) (Supplemental Figure S1b). HVEM expression was also analyzed after administration of control (no treatment), anti-PD-1 alone, anti-BTLA alone or combination therapy. There was no significant difference in HVEM expression on tumor-infiltrating CD11b+ cells, CD11 c+ cells, or CD19 + B cells with the four treatment arms. There was significantly higher HVEM expression on CD3 + T cells with anti-BTLA (P = .0135) or combination therapy (P = .0285) compared to control (Supplemental Figure S1c).
A review of pulmonary toxicity studies of nanocellulose
Published in Inhalation Toxicology, 2020
Takafumi Sai, Katsuhide Fujita
The mechanism of inflammation induced by NC has been evaluated. The findings illustrated that inflammation and cell death are basically induced by oxidative stress due to the increased production of reactive oxygen species (ROS) in mitochondria (Farcas et al. 2016; Shvedova et al. 2016). This is the same mechanism by which inflammation is induced after non-NC exposure in alveoli (Tátrai et al. 1996). A prior report also suggested that NC induces Th cell differentiation to Th1 cells through the induction of CD11 expression on antigen-presenting cells such as macrophages (Park et al. 2018). In addition, two intracellular inflammation-inducing pathways have been reported by in vitro studies using human-derived immune cells (Despres et al. 2019; Wang et al. 2019). In one pathway, the NLRP3 inflammasome is activated by cathepsin B released into the cytoplasm from lysosomes following NC-induced membrane damage, and the other pathway involves the upregulation of an IL-1β precursor through NF-κB activation due to increased ROS production in mitochondria. These signals ultimately induce IL-1β activation by the NLRP3 inflammasome. In recent years, research on the mechanism of inflammation induced by NC has progressed.