Cellular immunocompetence in aortitis syndrome.
Cellular immunocompetence was investigated in 17 cases of aortitis syndrome (3 active, 14 inactive stage). Both the active and inactive groups demonstrated significantly lower interleukin-2 (IL-2) production than healthy volunteers. The active aortitis syndrome group produced significantly more interleukin-1 beta (IL-1 beta) than the inactive group. The proportion of CD11b+ CD8+ cells was significantly lower in the active aortitis syndrome group. Further, the proportions of CD11b- CD8+ cells and CD57+ CD16- cells in the aortitis syndrome patients were significantly higher than the healthy volunteers. These results suggest that there are intrinsic qualitative abnormalities in the T cells that produce IL-2 in aortitis syndrome. Pathogenesis of aortitis syndrome is considered as follows: during the active stage, diminished IL-2 production impairs differentiation and proliferation of suppressor T cells, thus creating abnormalities in the inhibitory functions of immunoregulation and promoting the proliferation of cytotoxic T and natural killer (NK) cells. This presumably initiates inflammation of the aorta and/or artery.[1]References
- Cellular immunocompetence in aortitis syndrome. Hosotani, A., Uchida, H., Teramoto, S. Acta Med. Okayama (1993) [Pubmed]
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