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Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
A number of chemicals have been shown to alter (most often as suppression) delayed-type hypersensitivity in animal models.63 This list includes lead, selenium, tetrachlorodibenzodioxin (TCDD), tetrachlorodibenzofuran (TCDF), methylcholanthrene, carbofuran, 2,4-dichlorophenol, polychlorinated biphenyls (PCB) and organotins. PCB exposure has also produced decreased DTH reactions in people. The extent of effects and mechanisms of immunotoxic chemicals have been the subject of recent reviews and chapters.29,63,101,102 Selected examples of immunotoxic chemical effects on ACD are given below.
Monoclonal Antibodies in the Treatment of Malignant Lymphomas and Chronic Lymphocytic Leukemia
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
The safety of mAb is mainly related to their origin and to the compound attached to them. Radiolabeled mAb have a greater hematological toxicity than naked mAb because of the effect of surrounding normal hematopoietic cells in bone marrow. Immunotoxins also have greater toxicity because of the release of the toxin. Some mAb such as alemtuzumab may have larger hematological toxicity because the target antigen (CD52, in case of alemtuzumab) is not restricted to lymphoid cells.
Special Problems in Structures of Drugs
Published in Joseph Chamberlain, The Analysis of Drugs in Biological Fluids, 2018
Immunotoxins are molecular conjugates formed by monoclonal antibodies linked to toxic agents, which then target particular cells; in therapeutics the targeted cells are tumors. A typical and possibly most common toxin used in this way is ricin A.303 The desired conjugates are prepared identically as conjugates for radioimmunoassay development and these large protein molecules will have characteristic problems for the development of analytical methods.
Polybia occidentalis and Polybia fastidiosa venom: a cytogenotoxic approach of effects on human and vegetal cells
Published in Drug and Chemical Toxicology, 2021
Marcel José Palmieri, Amanda Ribeiro Barroso, Larissa Fonseca Andrade-Vieira, Marta Chagas Monteiro, Andreimar Martins Soares, Pedro Henrique Souza Cesar, Mariana Aparecida Braga, Marcus Vinicius Cardoso Trento, Silvana Marcussi, Lisete Chamma Davide
The immune system plays a major role in maintaining the body healthy, responding to invading microorganisms, macromolecules, neutralizing defective cells, and controlling cellular processes. In order to maintain immunocompetence, our organism relies on many compensatory mechanisms to avoid its impairment facing a toxic agent. Here, we evaluated the effect of two Polybia venoms upon whole blood nucleated cells (Baniyash 2006). Although the effects observed here are not specifically immunotoxic, they can lead to alterations in immune system functioning. These alterations could result in both immunosuppression or to an exaggeration in immune responses. Despite the compensatory mechanisms, there is no secure levels of such adverse effects for our healthy (Descotes 2006). Our concerns involved events which the individual are exposed to multiple stings at once, or exposed daily being often stinged. In these cases, the individuals would be more susceptible to infectious diseases, could present hypersensitivity reactions, and a immune system less consistent, besides the possibility of abnormal cell divisions occurring more frequently.
Inhibition of neovascularisation in human endothelial cells using anti NRP-1 nanobody fused to truncated form of diphtheria toxin as a novel immunotoxin
Published in Immunopharmacology and Immunotoxicology, 2021
Shamsi Naderi, Reyhaneh Roshan, Mahdi Behdani, Fatemeh Kazemi-Lomedasht
Angiogenesis is a critical process in the proliferation and metastasis of tumor cells. Anti-angiogenesis therapy is a possible strategy for the inhibition of tumor growth and development. The therapeutic efficacy of anti-angiogenesis drugs is limited due to the resistance of tumor cells to such drugs. Various approaches including targeted therapy, have been applied to overcome this hallmark feature [1]. Targeted toxin therapies have been considered to be effective toward tumor cells, reducing the adverse effect on normal tissues and therefore improving the patient’s chances for survival. Immunotoxins (ITs) are typically molecules comprising an immune system antibody conjugated to a toxic molecule [2]. However, in immunotoxins, a targeting ligand can be derived from antibody or growth factors. After binding of the ligand to a target cell antigen, the immunotoxin internalizes into the cell, enables the toxin to transport to the cytoplasm and kill the cells.
Immune stimulatory effect of anti-EpCAM immunotoxin – improved overall survival of metastatic colorectal cancer patients
Published in Acta Oncologica, 2020
Yvonne Andersson, Else Marit Inderberg, Gunnar Kvalheim, Theodor Malmer Herud, Olav Engebraaten, Kjersti Flatmark, Svein Dueland, Øystein Fodstad
The immunogenic effect seems to depend on specific binding of the immunotoxin to tumor cells expressing its target antigen, followed by killing of accessible tumor cells. One might speculate that tumor cell killing of tumor cells in this way will cause release of tumor antigens, which is taken up by antigen presenting cell (DCs) in vivo. Immunogenic cell death of tumor cells also releases a plethora of strongly immunogenic molecules stimulating maturation of DCs that have taken up antigen. These DCs will go to the lymph nodes where antigen-specific T-cells can be primed. Activated T cells will then be able to leave the lymph nodes, attacking the tumor in the periphery [20]. The induction of inflammation is supported by the presence and increased levels of several cytokines in the serum of MOC31PE treated patients. We found increased levels of IL-12, required for the induction of IFNγ- and TNFα-producing Th1 cells and necessary for promoting potent cytotoxic T cells accountable for antitumor immunity [21]. IL-2, another cytokine induced by MOC31PE, has been shown to be crucial to the expansion of CD8+ T cells and particularly important for the functional maturation of activated T cells. The cytokine response could be caused by MOC31PE-initiated ICD factors, as supported by the observed release of (extracellular) HMGB1 from MOC31PE treated colon cancer cells [13].