Hypersensitive response, components

Newman, M.A., Daniels, M.J., Dow, J.M. The activity of lipid A and core components of bacterial lipopolysaccharides in the prevention of the hypersensitive response in pepper. Mol Plant-Microbe Interact 10 (1997) 926-928. 

Phytoalexins are an Important component of the plant disease defense reaction called the hypersensitive response. Successful pathogens have evolved methods for dealing with plant phytoalexins. Including suppressors of their production, detoxification of the phytoalexins and In some cases avoiding elaboration of substances, called elicitors, that would otherwise Initiate the defense reaction. Elicitors obtained from pathogens are of considerable utility for study of various aspects of plant biology because of their interaction with the products of plant disease resistance genes. Substantial information has been obtained on how elicitors are perceived by plant cells and how they function, but much remains to be done. Finally, elicitors may prove of value for the economic production of exotic plant secondary metabolites and as specific herbicides. 

The immune system is characterized by a unique distribution, and many of its components are located close to the principal sites of absorption, including the gastrointestinal tract, the pulmonary tract, and the skin. Therefore, the immune system is in a position to be exposed to potentially high concentrations of drugs and chemicals. This phenomenon is especially important in hypersensitivity responses where the primary portal of entry of the hapten can determine the specific site of the reaction. 

Hypersensitivity responses to povidone-iodine include a few clear-cut cases of anaphylaxis, generalized urticaria-angioedema, and contact dermatitis. Polyvinylpyrrolidone not iodine has been implicated as the offending component. 

Respiratory hypersensitivity is an adverse reaction in the respiratory tract driven by immune mechanisms such as IgE antibody mediated allergic responses. Other less well understood mechanisms that have an immune component are also involved in respiratory hypersensitivity. OA is one outcome of respiratory hypersensitivity. Respiratory hypersensitivity and OA to proteins are primarily mediated by IgE antibody with subsequent inflammatory cell infiltrates. This same mechanism is responsible for OA to specific LMW chemicals such as the acid anhydrides and platinum salts. However, the role for IgE mediated responses in OA to other LMW chemicals such as the isocyanates and plicatic acid is poorly defined and other mechanisms may be responsible. 

Autoimmunity. In autoimmunity, as with hypersensitivity, the immune system is stimulated by specific responses that are pathogenic, and both tend to have a genetic component that predisposes some individuals more than others. However, as is the case with hypersensitivity, the adverse immune response of drug-induced autoimmunity is not restricted to the drug itself, but also involves a response to selfantigens. 

It is unclear why certain foreign proteins can also stimulate the B-cells to secrete IgE antibodies, to result in allergy or hypersensitivity. The terms are used interchangeably, although the latter is usually restricted to milder forms of the response. The term anaphylaxis is used to describe the severe response (Box 17.4). Both reactions arise in genetically susceptible individuals and they are precipitated by exposure to environmental antigens such as pollen, some organic compounds, tobacco smoke, animal hairs or even components of some common foods such as milk and cereals. 

There is also a possibility that someone can develop a type IV delayed hypersensitivity to some monomers. Of the monomers used, TEGDMA and HEMA may have the highest incident of sensitivity, but that incidence is extremely low. Though there are no literature reports of toxicity to composite resins over the 30 years of dental use, there are investigations into the potential for at least an allergic response to degradation products or extractable components [181]. 

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