Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating immunoblasts were studied in 39 cases of ankylosing spondylitis. The results were compared with 20 normal subjects and a group of 39 patients with rheumatoid arthritis, Immunoblasts were found to be increased in 11 patients with ankylosing spondylitis and in 22 patients with rheumatoid arthritis in contrast to the controls who were found to have a normal lymphoid cell population in the peripheral blood. Fifteen patients showed raised levels of one or more class of immunoglobulin. Autoantibodies, including antinuclear factors, were negative in all cases. There was a correlation between raised immunoblasts and plasma viscosity but not with clinical assessment of activity. The increase of immunoblasts in the peripheral blood, together with the raised immunoglobulins supports the suggestion of an immunological basis for ankylosing spondylitis.
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PMID:Immunological reactivity in ankylosing spondylitis. Circulating immunoblasts, autoantibodies, and immunoglobulins. 94 71

Five patients with progressive fibrotic lung disease are described. The dominant symptom was slowly increasing dyspnoea, and cough and sputum were not prominent. Marked weight loss was also a feature. There was severe restrictive impairment of ventilation with normal arterial gas tensions. The changes were confined to the upper parts of the lung in some but others had more generalized disease. The duration has varied so far from two to 17 years. The lung changes are considered to be due to dense progressive fibrosis. Necropsy in two confirmed this. Histologically there was monotonous fibrosis with lymphoid collections and secondary bronchiectasis, a picture similar to that found in association with ankylosing spondylitis. None of these patients had joint disease. Tuberculosis was excluded as a cause by exhaustive bacteriological tests and the failure of chemotherapy to stop deterioration. All other recognized types of infective and non-infective progressive lung fibrosis were also excluded, and this is not considered to be a variant of cryptogenic fibrosing alveolitis. Though these patients have many features in common they do not necessarily have the same pathogenesis. They are presented as an encouragement to further study.
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PMID:Idiopathic progressive pulmonary fibrosis. 114 36

The pathogenesis of ankylosing spondylitis (AS) remains unknown, although previous studies have strongly suggested that it may result from immunological aberration. To further explore the pathogenetic mechanisms, in vitro syntheses of immunoglobulins and interleukin-2 (IL-2) by peripheral blood mononuclear cells (MNC), and the serum level of the interleukin-2 receptor (IL-2R) were studied in 35 patients with definite AS and in 28 healthy controls. MNC were cultivated in the presence of pokeweed mitogen (PWM) for seven days. Immunoglobulins in the supernatants were measured by rate nephelometer (Immunochemistry System Analyser II, Beckman.) In vitro synthesis of IL-2 was carried out by cultivating MNC in medium only; in medium containing physiological concentration of the male sex hormone i.e., testosterone 500 ng/dl and estradiol 2 ng/dl; and in medium containing physiological concentration of female sex hormone, i.e., testosterone 50 ng/dl and estradiol 20 ng/dl. IL-2 was quantitated using an IL-2-dependent cytotoxic T lymphoid cell line (CTLL). Serum IL-2R was measured using an IL-2R test kit (CELLFREE, T Cell Sciences, Cambridge, MA). The results showed: In vitro synthesis of IgG, IgA and IgM was significantly higher in AS than in controls; In vitro synthesis of IL-2 was significantly enhanced by testosterone in normal control, but not in AS; and Serum IL-2R was significantly elevated in patients with AS. These findings, viewed in conjunction with previous results here, lead to postulation that an inflammatory process, elicited in HLA-B27-positive males and caused by an infectious agent invading via the mucosa may both cause immunological abnormalities and provoke various symptoms and signs of AS.
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PMID:Elevated serum interleukin-2 receptor; increased in vitro immunoglobulin synthesis and lack of response to testosterone-enhanced in vitro interleukin-2 production in ankylosing spondylitis. 310 49

Few topics are more emotive than the use of radiotherapy for nonlethal diseases. Memories of Hiroshima and of patients with ankylosing spondylitis dying of leukaemia following irradiation haunt the physician. Nevertheless, there are exciting developments in our understanding of total lymphoid irradiation - a modality that results in striking immunosuppression. Should total lymphoid irradiation be used for rheumatoid disease?
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PMID:X-radiation in the management of rheumatoid disease. 389 Oct 2

It has been shown that HLA-B27 lymphocytes from healthy individuals (B27+ ankylosing spondylitis [AS]-), which are not lysed by an antiserum against Klebsiella K43, can be rendered susceptible to lysis after incubation in the culture filtrate of Klebsiella K43. This finding is compatible with a specific modification by a Klebsiella K43-derived soluble factor of a B27-associated lymphoid cell component. Preliminary characterization of the factor has indicated that it is nondialyzable, but it is heat labile at 56 degrees C for 30 min and has a 35,000-50,000 mol wt. The modifying factor activity of the filtrate is destroyed by neuraminidase but not by trypsin and alpha-chymotrypsin. Furthermore, the ability of the factor to convert B27+AS- lymphocytes can be specifically absorbed by B27+AS- lymphocytes, but not by B27+AS+, B27-AS+, or by B27-AS- lymphocytes, which suggests that B27+AS- cells carry a hypothetical receptor which can specifically bind a Klebsiella K43 antigenic determinant. These results imply that the modification by environmental agents of specific major histocompatibility complex-associated gene products may be an important element in the pathogenesis of the HLA-B27-linked seronegative arthropathies.
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PMID:Characterization of a factor(s) present in Klebsiella culture filtrates that specifically modifies an HLA-B27-associated cell-surface component. 615 68

In this paper, we report the presence on Epstein-Barr virus-transformed lymphoblastoid cell lines on platelets and on fibroblasts of an HLA-B27-associated cell surface complex (antigenically related to some antigens of Klebsiella K43 and K21) which is identical to or cross-reactive with the determinant present on the peripheral blood lymphocytes (PBL) of B27-positive patients with ankylosing spondylitis (AS). By contrast, no Klebsiella K43 markers could be demonstrated on the spermatozoa of B27+ AS+ individuals even though these cells expressed the HLA-B27 alloantigen. No B27-associated K43 antigen was detected on the erythrocytes of patients or of normal controls. The B27-associated membrane marker is still detectable on lymphoblastoid cell lines after 20 generations and on fibroblasts after about 10 generations. This finding implies that the continued expression of Klebsiella-modified B27 structure is generally determined and does not require the repeated exposure of the cell surface to Klebsiella antigen. These data suggest that certain non-lymphoid as well as lymphoid cells may be involved in the complex sequence of events leading to the clinical manifestation of AS.
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PMID:The distribution of a specific HLA-B27-associated cell surface component on the tissues of patients with ankylosing spondylitis. 617 70

Ocular inflammatory diseases and ocular adnexal lymphoid tumors have become less obscure and intimidating by virtue of our ability to study the infiltrates in these various diseases for their B-lymphocyte and T-lymphocyte composition. Comparisons are also possible between lymphocytic profiles in the peripheral blood and the precise composition of the in situ infiltrates within the ocular tissue themselves. The availability of monoclonal antibodies, which can determine T-lymphocytic subsets such as T-helper cells and T-suppressor/cytotoxic cells, natural killer cells, and monocytes-histiocytes, has provided a powerful technology for the delineation of the distinctive immune composition of the inflammatory infiltrates, as well as any possible disturbances in T-cell immunoregulation. B-lymphocytes produce immunoglobulins, which may be misdirected as autoantibodies in local or systemic autoimmune diseases. Immunoglobulin-mediated and therefore B-cell derived conditions include vasculitis, progressive cicatricial ocular pemphigoid, Mooren's corneal ulcer, scleritis, and hay fever and vernal conjunctivitis. Other diseases in which B-lymphocytes, their immunoglobulin products or immune complexes formed with presently unknown antigens are potentially at fault are chronic non-specific uveitis; iridocyclitis in Behcet's syndrome; Fuch's heterochromic syndrome, ankylosing spondylitis, and Reiter's syndrome; Graves' disease; and idiopathic inflammatory orbital pseudotumor and myositis. T-cells do not produce immunoglobins, but rather secrete lymphokines or interact directly with receptors or determinants on viruses or target tissues (eg. immunosurveillance against neoplasia); it is possible that some autoimmune diseases are the result of neo-antigens on the surfaces of host tissues that have been coded for by a cryptic inciting virus. T-cell diseases include phlyctenulosis graft rejections, graft versus host disease, and possibly sympathetic ophthalmia and temporal arteritis. Natural killer cells are involved in many of the same diseases as cytotoxic T-cells, except that the former require no period of sensitization (natural immunity), whereas cytotoxic T-cells must undergo an antigen-specific blast transformation (acquired immunity of the delayed hypersensitivity type). In many diseases in which B-cell derived auto-antibodies are at fault, there may be local tissue or systemic T-cell imbalances, with a reduction in T-suppressor cells and a relative augmentation in T-helper cells, thereby facilitating production of misdirected auto-antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:B- and T-lymphocytes in ocular disease. 623 70

The histological features of the synovial membrane of peripheral joints in ankylosing spondylitis are similar to those seen in rheumatoid arthritis. There is intimal cell hyperplasia, a diffuse lymphocyte and plasma cell infiltrate, and formation of lymphoid follicles. Peroxidase-antiperoxidase staining shows the presence of IgG-, IgA-, and IgM-containing plasma cells in ankylosing spondylitis. The percentage of IgM-containing cells is significantly lower in ankylosing spondylitis than in rheumatoid arthritis.
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PMID:Histopathology of the synovial membrane of peripheral joints in ankylosing spondylitis. 675 21

In the studies reported here, peripheral blood lymphoid cells from 14 ankylosing spondylitis (AS) patients and 14 normal control subjects were examined for immune responses to the mitogens concanavalin A, phytohemagglutinin-P and pokeweed mitogen, as well as to primate spinal ligament, disc, and sacroiliac cartilage whole antigens. AS lymphocytes responded normally to mitogens and did not proliferate on exposure to spinal antigens. Assay for released supernatant proliferation inhibitory factor, tested on human HeLa cells monolayers failed to detect lymphokine release by AS lymphoid cells during exposure to spinal antigens.
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PMID:Cellular immunity in ankylosing spondylitis. Lack of response to spinal tissue antigens. 684 94

Synovial fluid studies have been made on 43 patients with rheumatic disease. Lymphocytes separated by a 2-stage procedure were examined for the presence of activated large lymphoid cells or immunoblasts. Such immunoblasts were found in 19 of 21 patients with classical rheumatoid arthritis and 7 of 10 patients with seronegative polyarthritis, including patients with Still's disease, psoriatic arthritis, and ankylosing spondylitis. No immunoblasts were seen in synovial fluid from osteoarthrosis or in the inflammatory but nonimmune synovial fluid from crystal-induced arthritis. The presence of immunoblasts showed a correlation with the lymphocyte count in the synovial fluid but not with the total white cell count. Preliminary studies confirm the spontaneous metabolic activity of these cells by autoradiography and show them by scanning electron microscopy to have a villous surface membrane. Simultaneous peripheral blood studies showed a lower incidence of immunoblasts than in the synovial fluid. It is suggested that these cells originate in the synovial membrane. In view of the known migration characteristic of immunoblasts these cells may be important in the spread of immune arthritis as well as being markers of disease activity.
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PMID:Immunoblasts in synovial fluid and blood in the rheumatic diseases. 696 65


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