Brief note on Immunotoxicity and Integrated Function of Natural Killer (NK)

Francisco Oliveira^*
*Correspondence: Dr. Francisco Oliveira, Department of Medicine, University of Coimbra, Portugal, Email:

Editorial Note

The intentional use of two categories of immunotoxic chemicals exposes people to them. Chemotherapeutic drugs are the first of them, and they are widely used in cancer treatment. The second sort of pesticide is one that is used to actively suppress undesirable plant and microbial growth, as well as vermin (herbicides and fungicides)(insecticides, acaricides, and rodenticides). These agents serve to assist humans in both circumstances, but they also have unexpected repercussions, either as a side effect or as a result of environmental contamination. Hundreds of chemotherapeutic medicines are used to help cancer patients live longer lives. Only a few of the most prevalent agents are discussed in this chapter, which were chosen following the process stated in Section. Similarly, the number of pesticides is immense; however, these agents may be classed based on their fundamental structure, which can then be classified further based on the compound's chemistry.

Nickel exposure causes allergic responses, which are the most immunotoxic effects. In nickel-sensitive people, allergic skin responses are the most common. Nickel's immunotoxic effects have been studied in depth just a few times. Despite the fact that nickel sensitivities are the most well-known toxicological outcome of eating or being exposed to exceptionally high concentrations of nickel chloride and the resulting divalent nickel, nickel openness can also produce a multitude of other immunotoxic effects. Nickel chloride, for example, increased superoxide anion production and phagocytosis activity in crab hemolymph in one study. Inhalation is a typical route of exposure for humans in the workplace, resulting in skin allergies, lung fibrosis, and respiratory tract cancer. However, it should be highlighted that these examples required nickel-polluted environments.

A solitary or different intramuscular infusion of nickel chloride brought about a huge decrease in an assortment of safe cells and capacities in mice. The lymph proliferative responses to T-cell mitogens phytohemagglutinin and concanavalin A were repressed in the spleens of nickel chloride–injected mice, and the number of theta-positive T-lymphocytes was reduced. Natural killer cell activity was suppressed in vitro and in vivo experiments, but there was no substantial reduction in spleen cellularity or suppressor cell generation.

They are advantageous in that they investigate the entire context of NK function, and the effects of toxin exposure can be evaluated using endpoints relevant to human experience - infection and organism/tumor burden. Nonetheless, these tests have a number of flaws. They are costly in terms of time, money, and animals, to begin with. Host-resistance experiments require a different cohort of animals because the challenge organism alters the constitutional, histologic, and cytometric results that serve as the foundation for other screening assays. Furthermore, because mortality is often used as an endpoint in these experiments, a high number of animals may be necessary to provide appropriate statistical analyses at toxin levels with moderate immunologic effects. While extending the challenge dose range may improve sensitivity, more animal testing is required. To alleviate the issues associated with mortality endpoints, surrogates such as pathogen titer or tumour load can be used. This has the disadvantage of necessitating extra labour.

Second, their holistic nature renders host-resistance assays generic for NK cells in general, in lieu of in-depth examination. This is exemplified by the mouse CMV model, which is by far the best understood NK-related infection. In mice with the Ly49Hactivating receptor variation, NK cells are the only terminal effectors necessary to protect them against early mortality. The NK response, on the other hand, is totally reliant on functional TLR-dependent DC responses, as previously established. As a result, any immunotoxicity impacting the DC component would have an impact on the outcome. A possible counter-argument to this notion is that host-resistance experiments are utilised as 'tier II' investigations once in vitro proof of NK dysfunction is acquired, implying that any drop in host resistance must be due to the NK effect.