Inflammatory Bowel DiseaseRichard P. MacDermott, William F. Stenson |
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Page 65
... assays , such as the RAJI cell assay and C1q precipitation , for immune complexes it is difficult to find a normal individual without circulating immune complexes . 121 The question is thus not whether there are immune complexes in IBD ...
... assays , such as the RAJI cell assay and C1q precipitation , for immune complexes it is difficult to find a normal individual without circulating immune complexes . 121 The question is thus not whether there are immune complexes in IBD ...
Page 105
... assay , apparently by downregulating a CD4 + subset.89 This result might reflect that a suppressive circuit in the gut is initiated by HLA class II - dependent CD4 + cells17 ; and murine enterocytes have recently been shown to present ...
... assay , apparently by downregulating a CD4 + subset.89 This result might reflect that a suppressive circuit in the gut is initiated by HLA class II - dependent CD4 + cells17 ; and murine enterocytes have recently been shown to present ...
Page 204
... assay of intestinal biopsies . It is difficult to interpret these data because the majority of PGs that were measured presumably arose from the trauma associated with biopsy and tissue handling.33 Even if tissues are rapidly removed and ...
... assay of intestinal biopsies . It is difficult to interpret these data because the majority of PGs that were measured presumably arose from the trauma associated with biopsy and tissue handling.33 Even if tissues are rapidly removed and ...
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abnormalities acid action activity addition agents alterations antibodies antigens appear associated bacterial blood cause chronic Clin clinical colonic compared complement complex component Crohn's disease cytokines cytotoxic decreased defect determined diarrhea effects enhanced epithelial cells epithelium et al evidence expression factor findings function Gastroenterology genes genetic granulomas growth human immune immune response Immunol immunologic important incidence increased induced infection inflammation inflammatory bowel disease inhibition initially injury intestinal involved isolated lamina propria lesions leukocyte levels lymphocytes macrophages markers mast cells mechanisms mediators mononuclear mucin mucosal Nature neutrophils normal observed occur patients population possible potential present production prostaglandin protein rates recent receptor regulation relatives release reported response risk role schistosomiasis secretion secretory serum shown specific stimulation studies suggest T-cell tissue ulcerative colitis vitro