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.
Hosotani
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A
Second Department of Surgery, Okayama University Medical School, Japan.
Uchida
H
H
Teramoto
S
S
D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D001015:Aortic Arch Syndromes / Q000276:immunology*; D018959:CD57 Antigens; D016827:CD8 Antigens / Q000032:analysis; D005260:Female; D006801:Humans; D007121:Immunocompetence; D007375:Interleukin-1 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D016177:Macrophage-1 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D017452:Receptors, IgG / Q000032:analysis
D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D018959:CD57 Antigens; D016827:CD8 Antigens; D007375:Interleukin-1; D007376:Interleukin-2; D016177:Macrophage-1 Antigen; D017452:Receptors, IgG