Molecule-receptor binding defense

The three molecules of the IL-1 family, interleukin-la (IL-la), interleukin-1 3 (IL-ip), and interleukin-1 receptor antagonist (IL-IRa) map to the long arm of chromosome two in the human genome. It appears that the family arose via a gene duplication event some 350 million years ago, and the molecules possess between 27.5 and 36% sequence identity with each other (Table 2) [1,14,15]. In addition, the genes for the two IL-1 receptors IL-1R1 and IL-1RII [16,17], and an IL-1R accessory protein (IL-lRacP), which binds to the IL-1, IL-1 receptor complex [18], have been identified. Together, these molecules via their differential activity serve primarily to modulate the host defense mechanism. 

ECM is facilitated by small hyaluronic acid molecules implies a function in host defense, but has not been proven (106). Increased levels of hyaluronic acid were associated with colon inflammation, psoriasis, osteoarthritis, rheumatoid arthritis, and scleroderma (101,107,108), as well as with viral infections (109). Hyaluronic acid is produced by endothelial cells and binds to its receptor, CD44, expressed by activated T and B cells, inducing the attachment of the two cell types (110). This interaction is controlled by the expression of specific hyaluronic acids sub-types or by modifications of CD44 on platelets (111). High molecular weight hyaluronic acid and CD44 are essential for scarless embryonic wound repair (112). 

The rules of Paracelsus, our old friend from chapter 1, help to put the body s defensive mechanisms into a more robust context. The magnitude of the impinging wave of toxic molecules, in most circumstances, directly influences their effect. At low exposure doses, the number of toxic molecules interacting with biological receptors is so few that no adverse impact develops. This can be due, in part, to an insufficient number of molecules binding to the receptor of the... 

Pesticides follow the rules of absorption as described in chapters 4 and 5 of this book. The receptor site, loosely defined, is what is in contest, with the toxic molecules moving to bind to it, while the cellular defenses attempt to prevent that from happening. There are at least two primary mechanisms by which that binding can be thwarted, and the development of pesticide resistance in insects has examples of both. One strategy is to alter the receptor site so that the toxic compound can no longer bind to it. The second strategy is to deploy proteins within the cell that either convert the pesticide into a relatively nontoxic metabolite or reduce the sensitivity of the target site for the pesticide. 

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