When a patient develops reactive arthritis after Yersinia enteritis, the following conditions are often fulfilled: the patient is HLA-B27-positive; however, some B27-negative individuals develop severe arthritis and some positives do not, in the initial phase, the diarrhea is milder, the anti-Yersinia antibody response of IgG class is more vigorous and persists longer, the anti-Yersinia antibody response of IgA class is more vigorous and persists much longer, the anti-Yersinia antibodies of IgA1 and IgA2 subclass, those with J-chain and, especially, those with secretory piece are produced more vigorously, indicating local immunostimulation close to the intestinal epithelium, in the early phase, Yersinia-IgM immune complexes are found in the circulation, and the lymphocyte transformation response against not only Yersinia but also against other gram-negative enteric bacteria is weaker. When all these aspects are considered together a strong suspicion arises that the patients who are destined to develop reactive arthritis fail in their first line of defense against the invading organism when contracting a Yersinia enteritis. This may lead to persistence of the microorganism within the body, e.g., in the intestinal epithelium or in the mesenteric lymphoid tissues, maintaining a stimulus for a prolonged--apparently futile and perhaps harmful--antibody production. Finally, the initiating and decisive factor should not be forgotten: the Yersinia. Why and how it triggers the process is at present one of the enigmas of the pathogenesis of reactive arthritis.
MRI of the brain and liver using T2 relaxation time measurements and proton spectroscopy (1H-MRS) of the brain was performed in four siblings with Wilson's disease (one with clinical disease and three asymptomatic) as well as age- and sex-matched control subjects. The T2 values of the liver were correlated with liver biopsy results. 1H-MRS of the left and right globus pallidus was obtained. The patient with clinical disease was examined three times, and two of three asymptomatic siblings twice. MR images of the brain were abnormal in all four patients. High signal intensity areas in the posterior thalamus, general atrophy and pontine myelinolysis were present in the patient with clinical manifestations. The T2 measurements of these areas confirmed the results of image analysis. Apart from general brain atrophy, the changes in the patient with clinical disease were largely reversible. The T2 values were significantly different from those of the control subjects only in the globus pallidus. The NAA/Cho, NAA/Cr and Cho/Cr ratios from the 1H-MR spectra of globus pallidus showed no significant difference between patients and control subjects. The mean values of NAA/Cho and NAA/Cr were lower in patients with Wilson's disease than in the control subjects. One of the patients had hepatic steatosis, but the liver T2 values were no different to those of the control subjects. In conclusion, the MRI findings reflect the success of the specific therapy in patients. MRI thus seems to be useful in the follow-up of Wilson's disease.
We evaluated the performance of new enzyme immunoassay (EIA) kits (Pyloriset; Orion Corporation, Orion Diagnostica, Espoo, Finland) for the detection of immunoglobulin G (IgG) and IgA antibodies to Helicobacter pylori in serum. Serum samples from 195 patients with upper abdominal complaints were collected. Biopsy specimens of the gastric mucosae were taken for histological analysis and bacterial culture. The sensitivity, specificity, positive and negative predictive values, and efficacy of the Pyloriset EIA-G in detecting IgG antibodies to H. pylori were 92, 84, 88, 90, and 89%, respectively, when compared with those of the reference methods used. The corresponding data for detection of IgA antibodies were 80, 89, 89, 79, and 84%, respectively. The overall prevalence of defined H. pyloni positivity was 54%. Moreover, the antibody tests showed a very good correlation with the biopsy findings. IgG antibodies were found in 93% of sera from patients with documented gastritis and H. pylori positivity, whereas only 4% of the sera from patients with documented gastritis and H. pylori-negative patients was positive. The results obtained for IgA antibodies were 81 and 6%, respectively. We conclude that the Pyloriset EIA-G, the test for IgG antibodies, is a good and reliable test for the detection of antibodies to H. pylori and as an indication of H. pyloni infection. The determination of IgA antibodies may be used as a test that complements the IgG antibody assay.
The ability of lymphocytes to recognize and bind to high endothelial venules (HEVs) is esstial for lymphocyte mition from the blood into ymphd tissues and into sites of mmation. Endothelial cell biding capacity also critically determines the clinical uselness of T-cell lines and clones in immunotherapy. In the present study, interleukin-2-dependent T-cell lines were derived from the blood, lamina propria of the gut, Aed synovium, synovial fluid, and peripheral lymph nodes. After 3-8 weeks of culture, the expression of homing-ated molecules and bing to mucal, synovial, and peripheral lymph node HEVs were analyzed. Cell lines derived from the blood and mu sal sites bound infcantty heifer to mucosal and synovial HEVs than to peripheral lymph node HEVs. MATERIALS AND METHODSGeneratio of Human T-Cell Lines. Human PBLs and synovial fluid lymphocytes (the latter drawn from arthritic patients) were isolated by Ficoll/Hypaque gradient centrifugation (Pharmacia). Lamina propria lymphocytes were isolated from surgically resected bowel specimens and from gut biopsies. Nine specimens were from histologically normal and six were from inflamed areas of the bowel. Surgically resected tissues were treated as described (11). Briefly, mucosa was dissected and treated with 0.5 mM EDTA to remove epithelial cells. Lamina propria lymphocytes were then released by overnight stirring at 370( in Hanks' solution containing collagenase type II (20 units/ml) and isolated by Ficoll/Hypaque gradient centrifugation. Ileal biopsy specimens were extensively washed and then cut to "'4-mm3 pieces. When incubated in the culture medium (see below) in 96-well microtiter plates, lymphocytes grew out from the biopsy specimens within a few days, and then the stromal remnants were removed from the wells. Eventually, all the contaminating cell types died and pure lymphocyte cultures were obtained. Peripheral lymph node lymphocytes were isolated from surgically resected nodes, later determined to be histopathologically normal, and synovial membrane lymphocytes were isolated from inflamed synovectomy specimens. Normal human appendices were obtained from explorative laparotomies.Lymphocytes isolated from the blood, synovial fluid, synovium, gut, and peripheral lymph nodes were cultured in Abbreviations: HEV, high endothelial venule; IL-2, interleukin 2; PBL, peripheral blood lymphocyte; VLA-4, very late activation antigen 4; LFA-1, lymphocyte function-associated antigen 1; TIL, tumor-infiltrating lymphocyte; mAb, monoclonal antibody; RAR, relative adherence ratio.tTo whom reprint requests should be addressed. 11436The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
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