Objective: To compare the incidence and clinical characteristics of tuberculosis (tbc) between patients with systemic lupus erythematosus (SLE) and kidney transplantation (KT) recipients. Methods: Six hundreds and twenty-two patients who were diagnosed as SLE from 1990 to 2001 in Kang-Nam St. Mary`s hospital were reviewed, retrospectively. As a control group, 347 kidney transplant recipients in the same center were evaluated. The extent of tbc was categorized into two groups: (1) limited disease (2) extensive disease. Cumulative steroid dosage and disease activity index including SLEDAI, serum complement levels, and anti-dsDNA titers were compared between the two groups. Results: The cumulative incidence rate of tbc was similar in both groups (37 cases and 5.7% in SLE versus 17 cases and 4.9% in KT). Mean interval from SLE diagnosis or KT to tbc development was not different between the two groups. The most common site of tbc was lung/pleura, and the others included lymph nodes (2 cases), knee joint (1), bone marrow (1), critecentral nervous system (1), kidney (1), colon (1), liver (1), and skin (1) in SLE. In contrast, most of tbc (16/17) developed exclusively in the lung and pleura in KT recipients. Cumulative doses of prednisolone 1 or 6 months before tbc diagnosis were not different between the two groups. Interestingly, extensive disease tended to be more frequent in SLE patients than in KT recipients although immuno-suppressants such as cyclosporine and azathioprine were more frequently administered in KT recipients. There were no differences in disease activity index including SLEDAI, complement levels, and anti-ds DNA titers at the time of tbc diagnosis as well as in the cumulative doses of steroid between extensive and limited diseases of tbc in SLE. Conclusion: The cumulative incidence rate of tbc was higher in SLE patients than in general population. The patterns of tbc tended to be more extensive in SLE compared to KT recipients in whom a stronger immuno-suppression was required, suggesting that immune dysfunction implicated by SLE itself may play an important role in determining the incidence and patterns of tbc infection.
Objective: To investigate the dosage of bovine type II collagen (BnCII) for the induction of oral tolerance in CIA animals, and to verify the changes of immune response and TGF-β production of mesenteric lymph node cells in tolerized CIA animals. Methods: Oral tolerance was induced by feeding of variable doses (5㎍, 10㎍, 20㎍ and 40㎍) of BnCII to DBA/1 mice 4 times per week during 2 weeks, and control mice were given ovalbumin (1000㎍), before immunization. We examed clinical assessment; incidence of arthritis, severity of arthritis, arthritic limb by visual analysis. IgG antibodies to BnCII were measured by ELISA, T cell responses to BnCII and PHA were quantified by antigen (CII)-induced 3H-thymidine incorporation into lymphocytes of mesenteric lymph node, draining lymph node, and spleen. TGF-β in supernatants obtained from lymph node culture medium was measured by ELISA. Results: Arthritis limbs were observed in 100% of control at 5 weeks after subcutaneous BnCII injection. The incidences of CIA in all tolerized group were significantly lower than that in control 5 weeks after immunization (control 100% vs. 5㎍ feeding group: 50%, 10㎍ feeding group: 50%, 20㎍ feeding group: 50%, 40㎍ feeding group: 55.5%, P<0.01). In comparison to control, mean articular indices were lower in all tolerized groups (control 5.13: 5㎍ feeding group 3.50, 10㎍ feeding group 2.75, 20㎍ feeding group 2.87, 40㎍ feeding group 2.63, P<0.05). Arthritic limbs were also significantly lower in tolerized groups (control 58.3: 5㎍ feeding group 20.8, 10㎍ feeding group 16.7, 20㎍ feeding group 20.8, 40㎍ feeding group 20.8, P<0.05). The titers of IgG antibody to CII were lower in tolerized group than that in control [tolerized group; median 10 (min. 0, max. 48), control; median 33 (min. 8.6, max. 101), P<0.05]. The proliferative responses to BnCII were significantly suppressed in tolerized (control 8010±2319cpm, tolerized group 4500±2060cpm, P<0.01). High TGF-β production was noted in tolerized group (control; 28pg/ml, BnCII feeding group; 73pg/ml). Conclusion: Oral tolerance in DBA/1 mice was successfully induced from low doses of BnCII (5㎍) and suppressed T and B cell function in conjunction with increased TGF-β production may play an important role for the induction of CII induced oral tolerance in DBA/1 mice.
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