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Of Japanese and English Mice

A Story of Interleukins and TNF Genes

Majid Ali, M.D.

 

Interleukin-1 and tumor necrosis factor á (TNF-á) are potent pro-inflammatory cytokines and play key roles in the pathogenesis of inflammatory autoimmune disorders, including Crohn's colitis, rheumatoid arthritis, and vasculitis.29-34 The occupation of interleukin-1 receptors on the cell membrane of inflammatory cells by interleukin-1 initiates several pro-inflammatory molecular events, including the generation of nitric oxide, prostaglandins, chemokines (small polypeptides that are chemotactic for neutrophils, macrophages, and lymphocytes).

Interleukin-1-receptor antagonist, a member of the interleukin-1 family, is a naturally occurring inhibitor of interleukin-1-receptors. By contrast, the occupation of interleukin-1 receptors by interleukin-1-receptor antagonists prevents all those events, simply by preventing the union of the two molecules. That is an excellent example of how molecular systems operate to preserve immunity by self-regulation and collaboration among the pro- and anti-inflammatory components. In health, interleukin-1 stays ready to evoke the inflammatory response and recruit inflammatory cells when that is called for. The interleukin-1-receptor antagonist also stays prepared to oppose excessive activity of interleukin-1 and prevent unregulated and destructive inflammatory responses. In cases of runaway inflammation—in Crohn's colitis and rheumatoid arthritis, for instance—the interleukin-1-receptor antagonist lags behind, and the inflammatory process becomes unrelenting.

Consistent with the above theoretical considerations, in two recent controlled trials administration of recombinant human interleukin-1-receptor antagonist to patients with moderately severe rheumatoid arthritis resulted in significant abatement of local inflammatory responses.35,36 However, the periods of follow-up were short and it is likely that such effects will be less impressive with time since the interleukin-1/interleukin-1-receptor antagonist system represents but one of the many known—and undoubtedly many more as yet unknown—systems of opposing molecules involved in immunity.

The story of the interleukin-1/interleukin-1-receptor antagonist system does not end there. In two recent studies, two entirely different types of inflammatory autoimmune disorders developed spontaneously in knock-out mice with targeted genetic deletion of genes for interleukin-1-receptor antagonist. In the Japanese study,37 the knock-out mice developed inflammatory arthropathy similar to rheumatoid arthritis, whereas in the English study the outcome was a lethal form of inflammatory arteritis. The arthritic mice produced large quantities of immunoglobulins, antibodies to type II collagen and double strand DNA, and a ten-fold increase in the levels of interleukin-1 messenger RNA in the joints. Extensive deformities of joints with erosions of bone and neutrophilic infiltrates developed by age 13 weeks. In the English study, the mice developed disseminated acute and chronic vasculitis with areas of marked arterial stenosis accompanied by hemorrhage and infarction in multiple organs.38 The effects on the vascular endothelium and muscularis were consistent with the known effects of interleukin on those organs. It has been speculated that the difference may be attributable to differences in the normal flora in Japan and England or genetic differences between the colonies of mice used. What may be the significance of those two entirely different outcomes in mice with deletion of the same gene? Future work is likely to show, as has been the case with the past studies, that there are many other variables in the system. It will be difficult to predict the biologic consequences of therapies based on loss-of-function and gain-of-function genetic manipulations. The advances in genetically designed therapies will exact unexpected tolls far in excess of, say, the problems caused by microbial resistance to antibiotics or pesticide treatments of crops during the last fifty years.

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* Genetics

* Re-Thinking DNA

* Intelligent language of Genes

* Junk DNA or Treasure trove

* Genes Know Their Neighbors

* A Story of Interleukins and Tumor Necrosis Factor

 

 

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