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Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
We learned in this chapter that Toxocara canis encodes a protein that is similar in structure to a host protein called CD23. The normal function of CD23 is to act as a receptor for the Fc region of IgE molecules on the surface of mast cells and basophils. Its precise value to T canis is unresolved. It may help to make the parasite appear more “host-like” Alternatively, it may bind the Fc region of IgE antibodies that might ordinarily damage the parasite by binding it with its Fab region. Can you describe an experiment which might allow a researcher to determine which of these two possibilities, if either, is more important?
Endothelins in the Lung
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Peter J. Henry, Roy G. Goldie, Douglas W. P. Hay
It is important to note that inflammatory cytokines and mediators previously implicated in asthma are released from inflammatory cells in response to ET-1. For example, ET-1 caused mast cell activation in the presence of IL-4 (44) and potently stimulated human monocytes to release IL-6 (45). However, several proinflammatory mediators are also known to stimulate the release of ET from airway cells, consistent with the notion that ET is a mediator in asthma. For example, in primary cultures of human airway epithelial cells derived from individuals without airway inflammation, II-1,11–2,11–6, and IGF-1 elevated levels of the ET-1 precursor bigET-1 (36). Furthermore, II-lα, II-1β, and TNF-α stimulated the expression of mRNA for preproET-1 and the release of ET-1 (36). These cytokines also elevated mRNA levels for preproET-1 in human bronchial epithelial cells (28). In addition, bronchial epithelial cells from asymptomatic asthmatics synthesized and released ET-1 in response to II-1β and histamine (4). 11–8, TNF-α, and TFG-β may also stimulate ET-1 release from cultured airway epithelial cells (33). The influence of these cytokines on ET-1 synthesis and release is likely to be significant in inflammatory respiratory diseases such as asthma. Interestingly, CD23-positive (low-affinity receptor for IgE) epithelial cells from a group of allergic asthmatics subjects responded to IgE by releasing ET-1 (46).
Molecular Mechanisms Controlling Immunoglobulin E Responses
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Rachel L. Miller, Paul B. Rothman
Further, considerable evidence has accumulated supporting the model that the pathogenesis of IgE-mediated allergic diseases, such as rhinitis and extrinsic asthma, involves heightened Th2 mediated immune responses. For example, the great majority of allergen-specific CD4+ T cell clones derived from peripheral blood lymphocytes of patients with allergies express a Th2 and Th0 phenotype consisting of high levels of IL-4 and IL-5, and little or no production of IFN-γ [29,30], Interleukin-4 and IL-5, but not IFN-γ, levels are elevated in sera of patients with allergic asthma [31,32]. Also, allergic asthmatics’ peripheral blood possesses an increased number of B cells bearing the IgE receptor CD23, which is evidence of B cell activation and IL-4 and IL-13 up-regulation [33].
Primary Ciliary Body Marginal Zone Lymphoma Presenting as Hemorrhagic Hypopyon
Published in Ocular Immunology and Inflammation, 2021
İrem Koç, Hayyam Kiratli, Yasemin Kapucu, Fatma Gündoğdu, Arzu Sağlam
Histopathologic examination of the specimen revealed a lymphoid infiltrate composed of monocytoid small lymphoid cells and plasmacytoid cells (Figure 2). Immunohistochemical analyses showed that these cells were positive for CD20 and displayed monotypic staining for lambda light chain. All lymphoid cells stained positive for BCL 2. CD23 staining for follicular dendritic cells highlighted the irregular expanded dendritic network. BCL 6, CD10, CD5, SOX11, kappa, and Cyclin D1 stains were negative. The diagnosis of primary extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) was made based on these findings. The patient was treated with rituximab (750 mg) and cyclophosphamide (50 mg) monthly, for 6 months. During 12 months of follow-up all anterior segment findings totally subsided (Figure 3), and there was no evidence for local recurrence and systemic involvement.
IgG4-rich reactive lymphoid hyperplasia of the lacrimal gland
Published in Orbit, 2020
Norberto Mancera, Jasmina Bajric, Curtis E. Margo
The lacrimal gland was effaced by a proliferation of mostly small lymphocytes with primary and reactive follicles (Figure 2, upper left). No ductal or acinar cells were seen. Prominent mantle zones surrounding follicles were present (Figure 2, upper right). Plasma cells were found within interfollicular areas. There was a mixture of CD3 positive T-cells found within interfollicular regions and CD20 positive B-cells within follicles (Figure 2, lower panel 3). Relatively few tingible body macrophages were present within follicles. BCL-2, CD5, and CD43 positive cells corresponded to T-cells. Follicles varied in size and shape, best appreciated with the CD3 and CD20 stains. Cyclin D1 stains were negative. CD21 and CD23 expression displayed a follicular dendritic network. BCL-2 was not present in follicles. Ki-67 displayed normal pattern of polarization within germinal centers. Fibrosis and obliterative phlebitis were notably absent. In situ hybridization for kappa and lambda light chains showed a predominance of kappa chains (7:1). A B-cell gene rearrangement study was negative. The T-cell receptor gamma gene rearrangement was positive (later interpreted as secondary to reactive lymphoid process).8 Flow cytometry submitted at the time of surgery was polyclonal. Immunohistochemical stains for IgG4 were performed following the report of elevated serum level. The proportion of IgG4+ to IgG+ plasma cells ranged from 40% to 60% (Figure 3). IgG4+ plasma cells exceeded 20 per high-power microscopic fields.
Important roles of CD32 in promoting suppression of IL-4 induced immune responses by a novel anti-IL-4Rα therapeutic antibody
Published in mAbs, 2019
Jie Zhao, Liangfeng Jiang, Lan Deng, Wei Xu, Yang Cao, Chen Chen, Yan Yang, Huiling Wu, Yuping Huang, Zhenping Zhu, Haomin Huang
Multiple lines of evidence demonstrated that IgE production from B cells is negatively regulated by CD23.28 There are two isoforms of CD23, CD23a and CD23b. CD23a is exclusively expressed on human B cells, whereas CD23b is upregulated by IL-4 on a variety of hematopoietic cells, including B cells and monocytes. Using CD23 transgenic mice, Payet-Jamroz M et al. demonstrated that CD23 expressed on non-lymphoid cells provided B cells with signals that resulted in the decrease of IgE production.31 More recently, the Chan lab showed that signaling through CD23 on B cells differs from that of the monocytic lineage cells.32 They proposed that CD23 plays roles in the regulation of IgE synthesis in human B cells, whereas CD23 may regulate the phagocytosis of IgE and allergen in monocytes. These data suggest that, as a principal mediator of most type I allergic reactions, IgE production is tightly controlled by comprehensive cross-talk between B cells and surrounding non-lymphoid cells, in which CD23 plays key roles in response to IL-4. Indeed, conflicting observations were also seen for the roles of CD23 and IgE in the regulation of inflammatory responses in asthma, probably due to the complexity of the disease environment. The Borish lab showed that individuals with asthma displayed a much higher level of CD23 expression on monocytes relative to that of normal individuals,24 whereas the Weiss’ group demonstrated that the elevated IgE levels seen in asthmatic patients were associated with reduced CD23 expression.25 Therefore, the amount of IgE observed in our studies was most likely a net result from the manipulation of the global signaling of IL-4Rα, activating and inhibitory FcγRs on B cells and monocytes by anti-IL-4Rα antibodies.