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Macrophages As Effectors Of Cell-Mediated Immunity
Published in Hans H. Gadebusch, Phagocytes and Cellular Immunity, 2020
Experimental allergic encephalomyelitis (reviewed by Paterson265) is produced by immunizing animals with extracts of central nervous tissue in adjuvant, generally Freund’s complete adjuvant. An autoimmune reaction leads to demyelination not only in the central nervous system but also in the peripheral nervous system. Passive transfer studies have indicated the importance of cell-mediated immunity in the production of the disease.265,268 Observations by light microscopy269 and electron microscopy270,271 have linked the damage to the invasion of nervous tissue by mononuclear cells, but the mechanism of demyelination and the relative roles of humoral antibodies, lymphocytes, and macrophages have not been at all clear. Wisniewski et al.272 studied by electron microscopy demyelination in peripheral nerves of rabbits with acute experimental allergic encephalomyelitis. Lymphocytes and macrophages infiltrated the tissue, but demyelination was seen only when there was penetration of the basement membrane and cytoplasm of Schwann cells by cells with the ultrastructural characteristics of mac rophages. There was no evidence to suggest that macrophage penetration followed damage initiated, for example, by humoral antibodies or by lymphocytes.
Rabies and other lyssaviruses
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Thiravat Hemachudha, Jiraporn Laothamatas, Henry Wilde
In some parts of the world where nervous tissue rabies vaccine is still widely used, allergic encephalomyelitis must be included in the differential diagnosis. These vaccine-induced “accidents” develop in as many as 1 in 400 Semple vaccine-treated patients and less often in subjects who received mouse brain vaccine [3,4]. Neither phobic spasms, paresthesias at bite sites, nor fluctuating consciousness is present in these postvaccination reactions.
Commensal microbiota and its relationship to homeostasis and disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Jonathan Braun, Elaine Y. Hsiao, Nicholas Powell
Although one might intuitively anticipate that intestinal microbes exert influence over helper T-cell polarization in the gut, it is more surprising that gut microbes can modulate extraintestinal T-cell responses. Germ-free mice have impaired immunity and increased susceptibility to particular infections. However, they are also less sensitive to T-cell–mediated autoimmune conditions. Experimental allergic encephalomyelitis (EAE) is a frequently studied animal model of autoimmunity that mirrors aspects of human multiple sclerosis. Disease is mediated by T cells responding to antigens present on the myelin sheath that coats nerves. EAE can be induced in rodents and primates by immunization with nerve tissue–derived proteins or peptides, such as myelin basic protein or myelin oligodendrocyte glycoprotein in adjuvant. About 2 weeks after immunization, mice develop relapsing and remitting symptoms of weakness and paralysis. EAE is characterized by expansion of TH17 and TH1 cells in inflamed nerve tissue. It has been shown that germ-free mice are much less sensitive to EAE induction than mice colonized with a conventional intestinal microflora. Many germ-free mice failed to develop any neurologic features. EAE resistance in germ-free mice is associated with an attenuated inflammatory response. These experiments strongly implied that gut microbes are necessary for at least some pathogenic T-cell responses outside the gut (Figure 19.5).
Novel nano-carriers with N-formylmethionyl-leucyl-phenylalanine-modified liposomes improve effects of C16-angiopoietin 1 in acute animal model of multiple sclerosis
Published in Drug Delivery, 2023
Xiao-Xiao Fu, Han Qu, Jing Wang, Hua-Ying Cai, Hong Jiang, Hao-Hao Chen, Shu Han
As a disease of the CNS caused by inflammatory demyelination, experimental allergic encephalomyelitis (EAE) shares many clinical and pathological features with MS, and is considered a model of MS (Arnon & Aharoni, 2009). A previous study has indicated that chemokines can induce inflammatory processes and demyelination in both EAE and MS (Karpus, 2020). Among the previously established rodent models of EAE, the acute model using Lewis rats has demonstrated a single peak of paralysis followed by spontaneous recovery, which is a characteristic of MS (Eng et al., 1996). This acute model can be helpful to elucidate the immune response in MS induced by inflammation and to study novel therapeutic agents. The inflammatory response in MS is complex, and suppressing the inflammation is a crucial goal when developing effective treatments (Han et al., 2013). Of the available anti-inflammatory drugs, glucocorticoids have shown central efficacy in MS (Eng et al., 1996). Unfortunately, this class of potent anti-inflammatory drugs, including methylprednisolone, gives rise to several undesirable side effects related to immunosuppression.
Association of polymorphism -308G/A in tumor necrosis factor-alpha gene (TNF-α) and TNF-α serum levels in patients with relapsing-remitting multiple sclerosis
Published in Neurological Research, 2021
Antonia A. Grigorova, Anastasiya G. Trenova, Spaska A. Stanilova
Tumor necrosis factor-alpha (TNF-α) is a potent pro-inflammatory cytokine with a pleiotropic effect, involved in acute and systemic inflammation. Mainly TNF-α is produced by activated macrophages and Th1 lymphocytes as well as B-cells, NK cells, astrocytes, and microglia in the CNS [2]. TNF-α interacts with two cell-surface TNF receptors – TNFR1 (55kDa) and TNFR2 (75 kDa) and triggers the cell survival and pro-inflammatory NF-kB and MAP kinases activation. The soluble TNF-α binds the TNFR1 mediating chronic inflammation and apoptosis whereas transmembrane TNF-α binds to TNFR2 and thus activates genes for cell survival and chronic inflammation [5]. TNF-α mediates different signaling pathways, activated by their receptors, and exerts both physiological and pathogenic effects. The pathogenic function associated with higher levels of TNF-α includes the facilitation of inflammation and tissue damage which results in the activation of a cascade of inflammatory events, causing tissue disruption in autoimmune diseases [6,7]. Studies showed increased levels of TNF-α in the serum and cerebrospinal fluid (CSF) in MS patients as well as higher levels of TNF-α were found in active demyelinating lesions in CNS. Lots of evidence demonstrated the correlation between increased levels of TNF-α and the progression and severity of the disease [4,8,9]. The participation of TNF-α in demyelinating diseases such as experimental allergic encephalomyelitis (EAE) is considerably understood and a number of studies are focusing on the role of this pro-inflammatory cytokine in the pathogenesis of MS [2].
CD40 as a therapeutic target in Sjögren’s syndrome
Published in Expert Review of Clinical Immunology, 2018
Several studies have demonstrated prevention of autoimmunity initiation, slowing of autoimmune disease progression, reduced leukocytic infiltration, and end tissue damage through blockade of CD40L in murine models [3]. SLE, like pSS, is characterized by over-activation of both B and T cells. Anti-CD40L therapy has pronounced effects on B cell activation through sustained co-stimulatory blockade in murine models of lupus [10], and in lupus-prone mice, anti-CD40L treatment improved renal disease, and survival [6]. In experimental allergic encephalomyelitis, CD40L blockade reduced inflammation and tissue damage in brain tissue [3]. In mice with collagen-induced arthritis, anti-CD40L agent blocked joint inflammation development, production of anti-collagen antibodies, inflammatory cell infiltration in synovial tissue, and erosions of cartilage and bone [11].