A colon score derived from serum CEA, CA19-9, CK1 and MUC1 is a potential valuable non-invasive index that could be used for detection and screening early stage colon cancer patients.
Antigen antibody complexes are suspected to play a role in the pathogenesis of some of the lesions that result from schistosomiasis. To examine the effect of immune complexes on the immune system of mice experimentally infected with Schistosoma mansoni, we measured antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-mediated serum hemolysis in normal and infected animals. ADCC activity in infected mice was depressed compared to control mice. However, preincubation of spleen cells for 24 h in medium followed by washing restored ADCC activity. This suggested that a soluble factor(s), presumably immune complexes, was bound to the Fc receptors with resultant block in ADCC activity and this was removed in vitro during the 24-hour preincubation. Furthermore, the complement activity of mouse serum was markedly depressed in mice infected for 3 or 6 weeks. Again, the presence of immune complexes could explain this depression since immune complexes bind complement. We attempted to confirm and extend these findings with an immunoperoxidase-staining technique using antibody to S. mansoni antigen. Most of the granuloma formations identified in portal tracts and intestinal mucosa were composed of macrophages and epithelial cells surrounding a central nidus of schistosome egg. In addition, schistosome antigen was seen diffusely bound to some of the lymphoid elements in the lamina propria and many of these cells appeared plasmacytoid. Furthermore, large amounts of schistosome antigen were sequestered in the medullary cords of the mesenteric lymph nodes and in the Billroth cords of the spleen. This suggests that the antigen is conveyed to the lymph nodes and the spleen through the systemic circulation. Taken together, these findings suggest the circulating immune complexes are a feature of schistosomiasis and may well contribute to the associated immunopathology.
Lymphocyte chalone from the spleens of old BALB/c, young BALB/c and young NZB mice caused significant suppression of the proliferative response of BALB/c and NZB spleen cells to T and B mitogens, whereas lymphocyte chalone from old NZB spleen did not suppress. Lymphocyte chalone from young and old NZB mice was tested using different ages of NZB/NZW responding spleen cells; at all ages concanavalin A- and lipopolysaccharide-induced proliferation was suppressed less by the chalone from old NZB mice than from that of young NZB mice. The responding NZB/NZW cells were suppressed equivalently at all ages studied. The basis for the loss of lymphocyte chalone activity in old NZB mice remains unknown; however, it appears likely that this event has a role in the disturbance of the negative feedback control system which contributes to NZB autoimmune disease.
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