BACKGROUND: This study investigates the association of HLA antigens to inflammatory bowel disease (IBD), which is reminiscent of the simultaneous or subsequent presence of ulcerative colitis (UC) and Crohn's disease (CD) found in these patients, showing also the concomitant association of other autoimmune conditions. The aim of this study is to confirm the autoimmune origin of IBD and the immunogenetic basis of the disease. METHODS: The study concerns 18 consecutive patients of both sexes, aged 20 to 62 years, sharing the clinical criteria of IBD indicated by previous authors. Tissue typing for HLA antigens of Class I (A; B; C); and Class II (DR; DQ) was carried out by conventional serologic methods, comparing alleles frequencies with those of normal controls random selected by the chi-square test. The main immune functions and other laboratory tests were also done in all patients, to define the concomitant autoimmune condition. RESULTS: Immunogenetic analysis shows the significant increase in two HLA antigens: HLA-DR2 (50.0% vs 25.5% of controls); HLA-DR7 (44.4% vs 21.1% of controls). In particular, the association of HLA-DR7 to IBD is reminiscent of that found in a personal series of 54 patients with primary celiac disease (55.5% vs 21.1% of controls). The findings on immune functions show the high frequency of anomalies of cell-mediated immunity (62.5%) and humoral immunity (88.8%), associated with decrease in complement and increase in immune-complexes. These alterations were always correlated with the presence of HLA-DR2 and/or HLA-DR7. CONCLUSIONS: This study on immunogenetics of ibd does not separate UC and CD on genetic grounds, thus suggesting that common HLA Class II genes may predispose to an altered regulation of immunologic mechanisms in these disorders.
BACKGROUND: This study investigates the association of HLA antigens to inflammatory bowel disease (IBD), which is reminiscent of the simultaneous or subsequent presence of ulcerative colitis (UC) and Crohn's disease (CD) found in these patients, showing also the concomitant association of other autoimmune conditions. The aim of this study is to confirm the autoimmune origin of IBD and the immunogenetic basis of the disease. METHODS: The study concerns 18 consecutive patients of both sexes, aged 20 to 62 years, sharing the clinical criteria of IBD indicated by previous authors. Tissue typing for HLA antigens of Class I (A; B; C); and Class II (DR; DQ) was carried out by conventional serologic methods, comparing alleles frequencies with those of normal controls random selected by the chi-square test. The main immune functions and other laboratory tests were also done in all patients, to define the concomitant autoimmune condition. RESULTS: Immunogenetic analysis shows the significant increase in two HLA antigens: HLA-DR2 (50.0% vs 25.5% of controls); HLA-DR7 (44.4% vs 21.1% of controls). In particular, the association of HLA-DR7 to IBD is reminiscent of that found in a personal series of 54 patients with primary celiac disease (55.5% vs 21.1% of controls). The findings on immune functions show the high frequency of anomalies of cell-mediated immunity (62.5%) and humoral immunity (88.8%), associated with decrease in complement and increase in immune-complexes. These alterations were always correlated with the presence of HLA-DR2 and/or HLA-DR7. CONCLUSIONS: This study on immunogenetics of ibd does not separate UC and CD on genetic grounds, thus suggesting that common HLA Class II genes may predispose to an altered regulation of immunologic mechanisms in these disorders.