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)

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

A previous study demonstrated that interferon was present in the serum of 30% of the patients with systemic lupus erythematosus (SLE), which was significantly higher than the 4.5% found in normal controls. We also recently reported that interferon production was deficient from SLE mononuclear cells, which has been attributed to immunodeficiency of the lymphocytes. In this study, interferon measurement included lymphocytes obtained from peripheral blood (PB), synovial fluid (SF) and synovial tissue (ST) in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). PB from normal subjects (NS) was used as a control. The results showed with PHA stimulation, that the interferon level in PBL (L = lymphocyte) in NS (70.0 +/- 67.5) was significantly higher when compared with PBL in RA (27.9 +/- 21.6). However, there was no difference between PBL in NS and AS. With ConA stimulation, the interferon level was significantly higher in the PBL of NS (130 +/- 59) and as compared with the PBL in RA (83.6 +/- 53.5). The SFL in RA (67.8 +/- 31.1) and the STL in RA (77.2 +/- 93.2) were also significantly different. It is concluded that interferon production was deficient not only in PBL in RA, but also in SF and STL in RA. The reduced interferon production from PB, SF and ST lymphocytes in RA patients may be due to previous release or immunodeficiency. Lymphocyte interferon production was normal in AS, which suggests that the lymphocyte abnormality between RA and AS may be different.
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PMID:Interferon production from peripheral blood, synovial fluid, and synovial tissue lymphocytes in patients with rheumatoid arthritis and ankylosing spondylitis. 170 7

Because the etiology of IgA and IgG hyperimmunoglobulinemia in ankylosing spondylitis (AS) remains unknown, the cellular immune system has been further studied by measuring the lymphocyte and its subpopulations in peripheral bloods of 50 definite AS patients and 40 normal controls. The system's functions have also been assessed in terms of proliferative responses to phytomitogens (Con A, PHA and PWM) and autologous mixed lymphocyte reaction (AMLR). The following results were obtained: The number of lymphocytes, total T, active T, OKIa1, OKT3, OKT4 and OKT8 cells in peripheral bloods of AS patients decreased more significantly when compared to the normal controls. The ratio of OKT4/OKT8 also decreased. However, the number of OKT8 cells was normal in inactive stage. While the lymphocytes of AS responded hyperreactively to PWM (B-cell mitogen), the response to Con A (T-cell mitogen) was depressed significantly. AMLR was impaired in AS patients no matter whether monocytes or B cells were used as stimulators. The aforementioned changes were especially evident in the active stage and most of them returned to normal after the disease became quiescent. It is therefore concluded that the etiology of hyperreactivity of B-cells in AS may be caused by T-cell immune aberration as evidenced by depressed lymphoproliferative response to T-cell mitogen (Con A) and impaired AMLR and/or the hyperfunction of B-cells themselves.
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PMID:Lymphocyte aberrations in ankylosing spondylitis. 316 9

Synovial fluids from patients with rheumatoid arthritis (13 cases), ankylosing spondylitis (six), psoriatic arthritis (two), osteoarthritis (three) and rubella arthritis (four) contain interleukin-1 (Il-1) activity as measured in the CH3/He mouse thymocyte assay. That this activity is Il-1 was shown by: (i) the time course of thymocyte stimulation; (ii) failure of PHA blast cells to absorb out the activity; (iii) molecular weight of 15,000-20,000 daltons, and (iv) ability to stimulate prostaglandin E2 production from synovial cells. These results indicate that IL-1 is an important mediator in the inflammatory pathway of different types of joint disease.
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PMID:Cytokines and the chronic inflammation of rheumatic disease. I. The presence of interleukin-1 in synovial fluids. 660 91

alpha 1 antitrypsin (alpha 1 AT) deficiency is a common genetic disorder seen in about 10% of the population. It predisposes to the development of a large number of inflammatory and immunologic disorders including rheumatoid arthritis, systemic lupus erythematosus, juvenile chronic arthritis, anterior uveitis, ankylosing spondylitis, fibrosing alveolitis and emphysema. We have investigated immunologic function in subjects with severe alpha 1 AT deficiency and demonstrated serum mediated enhancement of lymphocyte response to PHA and increased zymosan activation of mononuclear cells and neutrophils as measured by their chemiluminescence. These patients also have accelerated delayed hypersensitivity responses and increased levels of factor B, C3 and C5 but normal levels of immunoglobulin and other complement components. Such abnormalities in immunoregulation demonstrate a tendency to hyperreactivity that may contribute to disease predisposition.
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PMID:Immunoregulation by alpha 1 antitrypsin. 697 7

A study of cell immunity was carried out in 23 patients with ankylosing spondylitis, 17 HLA B27 +, 6 HLA B27 --, 5 donors of normal blood carrying HLA B27 antigen and 50 controls, 7 methods were used together for a study of the markers of the blood lymphocyte membranes: rosette E, rapid rosette E, anti HTLA + X, surface immunoglobulins, PEA gamma and BEA gamma rosettes, determination of the monocytes after peroxidase staining. Stimulation of lymphocytes with mitogens (PHA, Con A, PWM) were carried out. There exists an increase in blood lymphocytes carrying HTLA + X in patients with ankylosing spondylitis HLA B27 and also in healthy carriers of the same antigen. During ankylosing spondylitis with HLA B27 --, a statistically significant reduction in T lymphocytes forming E and E rapid rosettes was observed; finally, a rise in the levels of circulating immune complexes detected by the PEG --C4 method was noted. The significance of these facts is discussed.
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PMID:[Cellular immunity during ankylosing spondylitis]. 745 98