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Management of Natural Rubber Glove Sensitivity
Published in Robert N. Phalen, Howard I. Maibach, Protective Gloves for Occupational Use, 2023
Natural rubber is elastic between 15°C and 30°C. Below or above this range of temperature, it gets hard or soft, respectively. Several manufacturing processes are used to modify these characteristics, and various chemical compounds are added to NRL during these processes. Among those, polymerization, or vulcanization, comprises a reaction between polyisoprene polymers and sulfur to improve elasticity and reduce plasticity. Vulcanization is accelerated through the addition of different substances called accelerators and activators. Other added substances include antioxidants, stabilizers, blowing, and coloring agents. These substances can be associated with type IV hypersensitivity and allergic contact dermatitis.
Immunologically Mediated Diseases and Allergic Reactions
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Kim A. Campbell, Caroline C. Whitacre
Type IV hypersensitivity is also known as delayed hypersensitivity since the obvious signs of these reactions are observed twenty-four hours or more after contact with the antigen. In contrast to the first three types of hypersensitivity, which are antibody-mediated, type IV hypersensitivity reactions are cell-mediated immune responses involving T lymphocytes and activated macrophages (Figure 10.7). The most commonly recognized form of delayed hypersensitivity is allergic contact dermatitits, best exemplified by the acute eczema that develops following exposure to poison ivy. Other common allergens that induce allergic contact dermatitis include rubber, nickel, fragrances, cosmetics, and topical antibiotics. The contact dermatitis that may develop following exposure of a sensitized individual to bath soap is a typical form of DTH (Figure 10.8). More severe forms of DTH reactions have been observed in certain disease states such as leprosy or tuberculosis, where the antigen is persistent and cannot easily be eliminated by macrophages.
Consumer Safety Considerations of Cosmetic Preservation*
Published in Philip A. Geis, Cosmetic Microbiology, 2020
Corie A. Ellison, Alhaji U. N’jai, Donald L. Bjerke
Skin sensitization, also known as delayed contact hypersensitivity, is an immunologically mediated allergic response and is classified as a type IV response according to the scheme of Combs and Gell (28). The key factors characterizing type IV reactions are typically delayed onset of symptoms that get worse over a 24–72-hour timeframe. The symptoms typically involve pruritis, erythema, and edema and can progress to vesicle formation. These symptoms can also spread beyond the site of application of the product. Type IV reactions are associated with IgG antibodies. Poison ivy allergic contact dermatitis is a classic example of delayed type IV hypersensitivity. One way type IV sensitization can be distinguished from the irritation responses discussed is that the poison ivy rash-like sensitization, intense itching, and vesiculation response will likely spread beyond the site of exposure of the chemical insult, while the irritation response (typically with less edema than sensitization) tends to be localized to the initial area of the insult, and the skin response will typically persist for a longer period. In addition, induction of skin sensitization is a permanent change because memory cells within the immune system will remember the original exposure and the individual may react to any future exposures to the allergen that are above the threshold for elicitation of allergic contact dermatitis.
Physiological responses to cisplatin using a mouse hypersensitivity model
Published in Inhalation Toxicology, 2020
David M. Lehmann, Wanda C. Williams
Using a weight of the evidence approach, we arrived at the conclusion that CDDP exposure likely triggered a type I hypersensitivity reaction. However, the possibility remains that the effects we observed relate to other mechanisms. For example, the distinction between the different hypersensitivity classes is not always clear cut. Importantly, type IV reactions can occur in the lung triggering induction of airway hyperreactivity (Garssen et al. 1991). Although type IV reactions were traditionally aligned with Th1 cells, there are type IV hypersensitivity subtypes mediated by CD8+ and Th2 T-cells. When mediated by Th2 cells, a chronic asthma condition associated with eosinophil recruitment to the lung can develop (Czarnobilska et al. 2007). Importantly, we did not observe any signs of a skin irritation followed by repeated topical exposure to CDDP over a 15-day period. Still, additional investigations using this model and other approaches (e.g. T cell subset determinations) are necessary to better understand the contributions of different hypersensitivity types to CDDP hypersensitivity.
Computed tomography in hypersensitivity pneumonitis: main findings, differential diagnosis and pitfalls
Published in Expert Review of Respiratory Medicine, 2018
Olívia Meira Dias, Bruno Guedes Baldi, Francesca Pennati, Andrea Aliverti, Rodrigo Caruso Chate, Márcio Valente Yamada Sawamura, Carlos Roberto Ribeiro de Carvalho, André Luis Pereira de Albuquerque
The inhaled particle must have an aerodynamic diameter between 1 and 3 μm to reach the pulmonary acini, depositing in the terminal airways and alveoli. With continuous exposure, a type IV hypersensitivity response occurs. There is persistent and unrepaired epithelial cell damage with stimulation of interleukin (IL)-12 secretion by macrophages, thus promoting the differentiation of lymphocytes into a T-helper cell 1 (Th1)-like response. Immunocomplexes bind to Fc receptors on the surface of lymphocytes, stimulating the production of ILs, mainly tumor necrosis factor (TNF)-α and IL-1. These stimulate Th1 lymphocytes to produce interferon-γ. The latter further stimulates the production of TNF-α, transforming growth factor-β, and IL-1, generating a positive feedback mechanism that culminates in the chemoattraction of fibroblasts, increased local production of collagen, interstitial remodeling, and, finally, fibrosis. Some authors also postulated that the inability of the lymphocyte to eliminate a given antigen would polarize the immune response to Th2, resulting in a greater chance of disease progression to chronic HP with fibrosis [13,14].
Understanding Retinal Vasculitis Associated with Brolucizumab: Complex Pathophysiology or Occam’s Razor?
Published in Ocular Immunology and Inflammation, 2022
Ashish Sharma, Nilesh Kumar, Nikulaa Parachuri, Sonali Singh, Francesco Bandello, Carl D. Regillo, David Boyer, Quan Dong Nguyen
Extensive uveitis work-up was negative in the cases published. An expert panel disproved the need for a systemic workup to find a probable source of an embolic occlusion.13 Furthermore, the involvement of only the injected eye (no bilateral event) and mean age-group makes it less likely to be due to immunogenicity secondary to systemic autoimmune mechanism. Interestingly, all 15 published cases were females. The ASRS communication revealed that 88% of the cases reported to the ReST committee were females. We agree that female preponderance is seen in cases of systemic autoimmune diseases although this limited data set cannot conclusively implicate any causative association. In the brolucizumab data, 8 out of the 15 case reports revealed an underlying presence of DM, arthritis or multiple sclerosis, all of which have some auto-immune pathophysiology. Three cases were reported in the patients having breast cancer. Rosenbaum et al., have shown that patients with retinal vasculitis rarely suffer from systemic vasculitis and it is more commonly associated with local uveitis.14 The systemic immune reaction may thus not be a causative factor but can be a predisposing factor in the reactions related to vasculitis post-brolucizumab. The recently published report from Iyer et al gives us the first histopathological evidence about the nature of inflammation in the vitreous of one such case.8 It concludes the presence of inflammatory cells to be in favor of a type IV hypersensitivity reaction. The report though didn’t analyze the histopathological sample from the vessels involved to provide conclusive evidence.