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The Effects Of Metallic Tin and Inorganic Tin on Plasma Cells*
Published in Nate F. Cardarelli, Tin as a Vital Nutrient:, 2019
Despite the intensity of the process, it was short-lived, peaking at 2 to 3 weeks and subsiding rapidly thereafter. In contrast, the granulomas persisted for many months. The distribution of the reaction depended on the site of inoculation. When tin was injected into the hind paws, the popliteal, inguinal, and lumbar lymph nodes were enlarged instead of the mediastinal nodes.
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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Testicular Tumor French surgeon, Edme Lèsauvage (1778–1852), gave an account of spermatic cord tumors in 1845. Interstitial cell sarcoma was described by German pathologist, David Paul von Hansemann (1858–1920) in 1895. Seminoma was described by French urologist, Maurice Chevassau (b 1877) in 1906. German physician, Ludwig Pick (b 1868), described arrhenoblastoma in 1905. Radical surgery involving the removal of lumbar lymph nodes and spermatic vein was described by Philadelphia surgeon, John Bingham Roberts (1852–1924) in 1902. Gynecomastia associated with testis tumors was noted by Bennetjudson Gilbert (b 1898) in 1940.
Merits and complexities of modeling multiple sclerosis in non-human primates: implications for drug discovery
Published in Expert Opinion on Drug Discovery, 2018
Bert A. ‘t Hart, Jon D. Laman, Yolanda S. Kap
There is a plausible alternative concept, according to which the cause of autoimmunity in MS lies inside the CNS, namely the formation of a primary lesion from which self-antigens are released [37]. Indeed, several studies indicate microglia aggregates a.k.a. microglia nodules in the white matter as the earliest histological manifestation of a lesion [53]. Such microglia nodules are associated with axonal degeneration [54], which is a pathological hallmark of progressive MS. Such observations indicate that the classical ‘outside-in’ concept of MS may need to be reformulated, as the basis of MS may be progressive degenerative pathology and that relapses may be induced by hyper-reaction of the immune system against released self-antigens [37,55]. Conceptually, the immune hyper-reactivity is caused by the interaction of genetic and environmental risk factors, infection in particular [37]. Data obtained in EAE mice, EAE marmosets, and MS patients show that the released self-antigens may be captured by APC in CNS draining cervical and lumbar lymph nodes where immune activation can take place [56,57]. Indeed, surgical removal of these lymph nodes from Biozzi ABH mice impairs the chronic relapsing EAE course induced with myelin/CFA [58].
Engineering polymeric nanocapsules for an efficient drainage and biodistribution in the lymphatic system
Published in Journal of Drug Targeting, 2019
Ana Sara Cordeiro, José Crecente-Campo, Belén L. Bouzo, Santiago F. González, María de la Fuente, María José Alonso
When analysing the lumbar lymph nodes, at the same time point, we observed a statistically significant higher accumulation of polyarginine and carboxymethyl-β-glucan NCs than of CS NCs (Figure 7(d,e)). These results may indicate that, besides the surface charge each polymer confers to the nanocarrier, the intrinsic specificities of the polymer used could also play a role in this process. On one hand, polyarginine NCs were found to drain well through the draining lymph node chain and to accumulate strongly in both lymph nodes under study. The efficient internalisation of polyarginine by immune cells has been previously described, and found to be higher than that of other polycationic polymers, which could explain these positive results [82,83]. On the other hand, carboxymethyl-β-glucan NCs, which seem to accumulate at lower levels in the popliteal lymph node, eventually accumulated in the following node, at similar levels than those observed for polyarginine NCs. It is possible that anionic NCs drain along the lymphatics under the pressure of lymph flow, instead of remaining stuck in the first draining lymph node. Comparative studies that might help explain this behaviour are still lacking in the literature. However, in the absence of these reports, we can speculate that the affinity of some APCs receptors for these polymers may lead to their increased accumulation in the lymph nodes more distant from the injection site. Similarly, other beta glucans in particulate forms have shown fast drainage to the lymph nodes upon injection in mice and specific co-localization with macrophages within those lymph nodes [84–86].
Ipilimumab: an investigational immunotherapy for glioblastoma
Published in Expert Opinion on Investigational Drugs, 2020
Gilbert Youssef, Jorg Dietrich
The central nervous system (CNS) has traditionally been thought to be an immune-privileged organ, based on unique features of the blood-brain barrier, absence of lymphatic drainage system, and its paucity of immune cells [10–12]. However, there is increasing evidence that the CNS has a delicate lymphatic system draining into cervical and lumbar lymph nodes [13,14], and that immune cells play an important role in the pathophysiology of various auto-immune, inflammatory, and degenerative neurological diseases [15–17]. Furthermore, microglia act as the main effector cells of the immune system in the CNS, and are able to induce cytotoxicity, phagocytosis, and T cell activation, through antigen presentation, directed against any offending particles [18]. However, the brain parenchyma remains immunosuppressive in nature, and the normal immune responses are shifted towards a type 2 CD4+ TH response, leading collectively to a suppressed cell-mediated immunity [19]. Moreover, malignant gliomas have various immunosuppressive properties characterized by the recruitment of immunosuppressive T regulatory cells (Treg) and expression of anti-inflammatory cytokines [20–23]. Although tumor-infiltrating lymphocytes (TILs) can be found in the perivascular areas and within the tumor tissue [24], they are usually inhibited by the GBM tumor microenvironment (TME). In fact, the T-cell responses are regulated by co-stimulatory and co-inhibitory signals. The latter restrict or reverse the stimulation of T cells, are termed checkpoint inhibitors and are abundant in the TME [25–27], allowing GBM to escape attacks from the immune system. The two main immune checkpoints involved in immunosuppression are programmed cell-death 1 (PD-1) and cytotoxic T-lymphocyte antigen-4 (CTLA-4). Both are expressed on the cell surface, and deliver self-inhibitory signals to effector T cells, while CTLA-4 is also expressed on Treg, further inhibiting effector T cells in a cell-extrinsic pathway [28,29]. They act in a non-redundant, serial manner [30,31]. CTLA-4 is expressed by all T cells [32], and is usually upregulated on Treg during an inflammatory process [33,34]. It is homologous to CD28, a co-stimulatory signal that activates effector T cells by binding to CD80 and CD86 receptors and has a significantly higher affinity than CD28 to these receptors [32,33]. While CD28 activates T cells, CTLA-4 reverses this early activation and inhibits further T cell stimulation and expansion [32,34]. On the other hand, PD-1 alters the motility and metabolism of already activated T cells [25].