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)

We report a study of lymphocyte subsets in experimental arthritis induced in Wistar Furth rats by native human type II collagen and muramyl dipeptide. This experimental arthritis shares similarities with both the spondyloarthropathies and rheumatoid arthritis. Peripheral blood T lymphocytes, primarily the CD4+ cells (p = 0.01), were lower in arthritic rats than in the controls, although the difference in the CD4/CD8 ratio was not statistically significant. Splenic CD4 cells were significantly (p = 0.03) more numerous in arthritic rats, while the numbers of MHC class II positive cells (p = 0.002) and kappa-bearing B-cells (p = 0.0004) were significantly lower. Determination of peripheral blood and spleen lymphocytes subsets could therefore be used for the assessment of arthritis and for the evaluation of therapeutic agents. Thymic T-cell differentiation does not appear to be impaired in this model. These results differ from the peripheral blood disturbances described in the active stages of human rheumatoid arthritis and are more similar to those reported in ankylosing spondylitis patients. However, the absence of alterations in the Peyer's patches suggests that pathogeneic mechanisms involving mucosal areas and exogenous intestinal antigens are not reproduced in this model.
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PMID:Lymphocyte subpopulations in an experimental model of axial and peripheral enthesiopathies. 148 9

Three patients, all exhibiting symptoms before 15 years of age, were diagnosed as juvenile ankylosing spondylitis (JAS) by stigma of JAS. The families of these three patients--a total of fifteen first-degree relatives--had clinical, radiologic and laboratory examinations. All three patients and four family members (26%) had positive HLA-B27 and ankylosing spondylitis (AS). Five (33%) of these three family members had positive HLA-B27 but were asymptomatic; six members(40%) were HLA-B27 negative and symptom-free. A high positive rate of HLA-B27 was found among the patients (100%) and the family members (60%). The rheumatoid factor, antinuclear antibody, and anti-native DNA antibody were negative for all patients and family members. Significant elevation of IgG, IgA, and C3 were noted in the AS group. The CD3 cell was lower, and the ratio of CD4/CD8 was decreased in the AS group. Lympho-proliferative responses to phytomitogens (Con A, LPS and PHA) were also done in our study. There was no significant difference in Con A and LPS stimulation index among the AS group, symptom-free family members and normal controls.
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PMID:Immunological study in three families of juvenile ankylosing spondylitis. 151 12

Several distinct arthritic syndromes now have been recognized in HIV-infected persons. These comprise seronegative spondarthritis, including classic Reiter's syndrome and psoriatic arthritis associated with HLA-B27, and undifferentiated arthritis usually confined to the lower limbs, unassociated with other lesions, and unrelated to any known genetic marker. In such cases great care should be taken to exclude infection. In addition, a syndrome of short-lived but sometimes severe arthralgias also occurs. Spinal pain is a major problem in some patients but ankylosing spondylitis appears to be rare among this group. Psoriasis probably occurs more often in the HIV-infected group than in the population in general and may be especially severe in those patients with arthritis. Arthritis has been reported in the United States, Europe, and Africa among persons considered to be at high and low risk for HIV infection. Arthritis can occur at any stage of HIV infection, but the true prevalence of arthritic syndromes and the nature of their association with HIV infection remains unclear. In view of the development of Reiter's syndrome in some patients, precipitating bacterial infections have been sought as the culprits. In a minority of cases, shigella, yersinia, and campylobacter infections have been implicated, but in the majority of cases, no specific infection has been identified. In most patients depletion of circulating CD4-positive lymphocytes is present by the time that arthritis is detected, but only limited data on synovial immunopathology are available. In some patients changes of nonspecific chronic synovial inflammation are present and synovial fluid cell counts are high. In other patients evidence of inflammatory changes is minimal. Human immunodeficiency virus has been isolated from joint fluid and identified in large mononuclear, probably dendritic, cells and lymphocytes. Synovium from patients dying with AIDS but with apparently normal joints also shows significant abnormalities that could lead to joint disease in long-term survivors. The possibility of a viral etiology of arthritis in some cases is suggested by the induction of arthritis in animals by lentivirus infection; it also is possible, however, that HIV enhances the effect of mechanisms that can operate in the absence of HIV infection. Conventional treatments of rheumatic lesions, including intraarticular steroids, appear to be safe and reasonably effective. Anecdotal evidence suggests that treatment with methotrexate and azathioprine leads to exacerbation of HIV disease and should be avoided.
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PMID:Reiter's syndrome and associated arthritides. 204 87

Monoclonal antibodies and flow cytometry techniques were used to analyze and compare the distribution of lymphocyte subpopulations of peripheral blood and synovial fluid (SF) from 70 patients, 43 with rheumatoid arthritis (RA), 10 with ankylosing spondylitis (AS) or reactive synovitis, 10 with psoriatic arthritis and 7 with other inflammatory arthritic diseases. Patients with RA had significantly reduced number of CD8+ T cells and greater CD4/CD8 ratios in peripheral blood, a greater number of CD4+ T cells and lower CD4/CD8 ratio in SF. No significant difference was found between the groups with AS, reactive synovitis and psoriatic arthritis. The simultaneous analysis of peripheral blood and SF lymphocyte subpopulations allowed us to establish a transsynovial lymphocytic ratio which reflects CD4/CD8 variations on both peripheral blood and SF, 2 easily accessible compartments for physicians. This new ratio may distinguish RA from other inflammatory arthritic diseases.
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PMID:The transsynovial lymphocytic ratio. Characterization of blood and synovial fluid lymphocytes from patients with arthritic diseases. 341 40

The T gamma-lymphoproliferative syndrome is characterized by a proliferation of large granular lymphocytes (LGL). It is often associated with neutropenia, and in 30% of cases with rheumatoid arthritis (RA). Phenotypic analysis has demonstrated that in most cases of RA with T gamma-proliferative disease, the LGL represent T cells with a clonal rearrangement of the alpha/beta T cell receptor (TCR2). Here, three patients with gamma/delta TCR1+ LGL proliferation suffering from long-standing arthritis and neutropenia are described. The first patient with RA showed an expansion of a heterogeneous CD2+ CD16+ CD56- LGL population, of which 30% coexpressed TCR1 with V delta 1 rearrangement. The second patient with ankylosing spondylitis and RA was suffering from proliferation of TCR1+ (V gamma 9-, V delta 1-), CD2+ CD16- CD56- LGL with low coexpression of CD8. The third patient with RA was suffering from a proliferation of TCR1+ (V delta 1+, V gamma 9-) CD4- CD8- CD16- CD56- lymphocytes. On the basis of these unusual findings, the pathogenetic role of TCR1+ T cells in RA is discussed.
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PMID:TCR1+ large granular lymphocyte proliferation in rheumatoid arthritis. 787 35

Expression of adhesion molecules, CD11a, CD11b and CD18, and of the function-associated molecules CD3, CD4, CD8, CD16, CD19, CD56 and CD57 was assayed on peripheral blood leukocytes from normal control subjects (n = 10), and from patients with adult periodontitis PD (n = 9), ankylosing spondylitis AS (n = 11) and rheumatoid arthritis RA (n = 14). A novel rapid fixation leukocyte preparation technique was used which prevents artefactual up-regulation of surface antigens. In RA patients, the percentage of CD18+ lymphocytes was decreased and that of CD11b+ neutrophils was increased. On lymphocytes the mean fluorescence intensity (MFI) of both CD11b and CD18 was decreased whereas that of CD57 was increased. In AS patients the percentages of CD11b+ lymphocytes and neutrophils were increased and CD18+ lymphocytes and neutrophils were decreased. On lymphocytes the MFIs of CD11b and CD18 were decreased, whilst that of CD16 was increased. On neutrophils the MFI for CD18 was increased. No significant differences (p < 0.01) were seen for the periodontitis patients. It is suggested that the antigen expression on peripheral blood cells from RA and AS patients is consistent with leukocyte activation.
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PMID:Leukocyte activation and function-associated antigens in inflammatory disease. 831 19

In this study we compared cytokine production and cell proliferation of immunocompetent cells derived from patients with ankylosing spondylitis (AS) to those from healthy blood donors using a whole blood assay. To this end, blood cell cultures were stimulated with the superantigens MAS (Mycoplasma arthritidis supernatant) and staphylococcal enterotoxin B (SEB) and the plant lectins phytohaemagglutinin (PHA) and concanavalin A (Con A). The number of white blood cells (WBC) and lymphocyte subsets were also determined. Cell proliferation and levels of interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) were measured after stimulation with the different mitogens. An ELISA test was used to analyse supernatant cytokine levels. Individuals with AS showed significantly lower IFN-gamma concentrations and markedly lower cell proliferation rates with all tested mitogens than healthy controls, while there was no significant difference in IL-6 synthesis. IL-1 beta levels were slightly impaired in the patient group, but only blood cell cultures stimulates with MAS showed a statistical significance. Furthermore, there was a significant elevation of leucocytes and lymphocytes in patients with AS resulting in higher numbers of CD4-positive cells, which implies a higher CD4:CD8 cell ratio. CD19- and CD8-positive cells were not significantly distinct compared to healthy controls. This deviation in cytokine levels and cell proliferation points to a suppression of T lymphocytes. A disturbed T-lymphocyte function may play a part in the pathogenesis of AS.
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PMID:Stimulation of whole blood cultures in patients with ankylosing spondylitis by a mitogen derived from Mycoplasma arthritidis (MAS) and other mitogens. 903 20

The topics discussed at this conference covered many aspects of the pathogenesis, epidemiology, diagnosis and treatment of rheumatic diseases, from the search of new therapeutic targets and evaluation of new diagnostic techniques to preclinical and clinical development of novel therapies. This contribution focuses primarily on two issues that dominated this meeting. First, a number of interesting studies presented during this conference examined the possible value of novel selective therapies directed against recently identified targets of the immune system including cytokines (TNF-alpha, IL-6, IL-15) and inflammatory cells, such as B cells, CD4(+) T cells or memory/effector T cells. Second, clinical experience with newer anti-inflammatory treatments, such as TNF-alpha-blocking agents or leflunomide, is growing judging by the number of reports of their use in clinical practice and new indications. Several studies presented at this meeting examined the value of currently licensed drugs in new indications, such as ankylosing spondylitis or psoriatic arthritis, or studied new combinations of drugs, for example, a combination of different biological treatments (e.g., anakinra, etanercept), in already established indications. Interestingly, the results of these studies were not always as expected, thus increasing the importance of these particular trials. The growing experience with some of these novel therapies clarify the role of these treatments in particular forms of rheumatic diseases and will help to develop guidelines for the use of these sometimes powerful but also possibly harmful agents in clinical practice.
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PMID:The Annual European Congress of Rheumatology: recent advances in the treatment of rheumatic diseases. Lisbon, Portugal, June 18-21, 2003. 1451 90

The lymphocyte-osteoclast interaction has recently been described. The aim of this study was to investigate the possible relationship between ankylosing spondylitis (AS) and bone metabolism. Bone metabolism was evaluated in the blood of 49 patients with AS by means of biochemical markers and bone mineral density (BMD) with a Lunar device. Bone formation markers, bone specific alkaline phosphatase (BALP), osteocalcin (BGP), bone resorption markers, pyridinoline (Pyd), deoxypyridinoline (Dpyd) and lymphocyte surface markers (CD3, CD19, CD4, CD8, CD16+56) were analysed with ELISA and flow-cytometry methods. The patients had significantly lower femoral neck and trochanter BMD than the controls. Dpyd concentrations were negatively correlated to CD3+% and CD3-/CD16+56% cells. Neither mineral nor hormone levels were significantly correlated with absolute T scores of BMD of the hip sites. BALP and BGP were negatively correlated to BMD when expressed as T scores. We conclude that AS is related to accelerated osteoclastic activity. Many lymphokines and growth factors produced by lymphocytes can influence osteoclastogenesis and probably play a role in rheumatologic/inflammatory disorders.
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PMID:Association of immune function with bone mineral density and biochemical markers of bone turnover in patients with anklylosing spondylitis. 1462 78

Previous studies have suggested that CCR4 is particularly important in the selective recruitment of various subsets of leucocytes in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). In this study, we examined the percentage of CD4(+)/CCR4(+) T cells within circulating lymphocytes in active ankylosing spondylitis (AS), RA and SLE patients. The clinical significance of CCR4 expression as well as possible associations between the expression and serum levels of tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma and interleukin (IL)-10 were also examined. Our results showed that the percentage of CD4(+)/CCR4(+) T cells was significantly elevated in AS and RA patients as compared with normal controls. The percentage was also significantly higher in SLE patients who had received no treatment with glucocorticoids or cytotoxic drugs (untreated SLE) than that in controls. In addition, the percentage of CD4(+)/CCR4(+) T cells showed significant positive correlations with the Bath ankylosing spondylitis disease activity index (BASDAI) in AS and with the SLE disease activity index (SLEDAI) in untreated SLE. Of all the cytokines examined, the elevated serum IL-10 level was closely correlated with the percentage of CD4(+)/CCR4(+) T cells in AS, RA and untreated SLE. These results suggest that CCR4 may be crucial in the pathogenesis of AS, RA and SLE. The percentage of CD4(+)/CCR4(+) T cells can serve as a useful marker for the activity of AS and untreated SLE.
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PMID:Increased CCR4 expression on circulating CD4(+) T cells in ankylosing spondylitis, rheumatoid arthritis and systemic lupus erythematosus. 1549 47


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