Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum adenosine deaminase (ADA) activity and peripheral lymphocyte subsets of patients with myasthenia gravis (MG) were simultaneously measured. The ADA activity in MG (n = 30) was significantly higher as compared with normal control (n = 150) and multiple sclerosis (n = 12) (P less than 0.05). The ADA activity of generalized MG was higher than that of ocular MG, while a significant elevation of ADA activity was observed in grade IIB as compared with grade I of Osserman's classification (P less than 0.05). A trend of high ADA activity was demonstrated in those whose disease had advanced to a severe degree associated with unstable clinical features (P less than 0.05). In addition, there was a significant elevation of ADA activity in patients who disclosed positive anti-Ach-receptor-antibody as compared with negative one (P less than 0.05). There was no specific trend among the proportions of the subsets of peripheral lymphocytes which could reflect the severity of MG, however, the proportion of OK Ia1+ tended to be higher with advancing the grade of MG. Interestingly enough, a close correlation was found between the ADA activity and the proportion of OK Ia1+ cells (P less than 0.05). From the above results, it was concluded that high ADA may be responsible for the pathophysiology of MG through the alteration of peripheral lymphocyte function.
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PMID:High serum adenosine deaminase activity and its correlation with lymphocyte subsets in myasthenia gravis. 208 34

The purine enzyme, adenosine deaminase, is essential for the maturation of lymphocytes, cell growth and normal immune function. Since adenosine deaminase has the highest activity in the thymus and in T lymphocytes, it is hypothesized that a defective or altered enzyme may be a cause of myasthenia gravis, a lymphoid dyscrasia. It is proposed that the alteration is on the non-catalytic portion of adenosine deaminase concerned with the normal immune function of T lymphocytes. Lymphocytes, particularly suppressor T lymphocytes containing a defective adenosine deaminase will function improperly. They will lose their normal immune regulatory function, allowing immunoglobulin-producing B lymphocytes to produce autoantibodies against the nicotinic acetylcholine receptor, with resultant induction and perpetuation of the autoimmune state. In an attempt to compensate for the defect, there may be hypertrophy of the thymus and lymphoid system, with overproduction of a defective adenosine deaminase. Since many of the functions of thymosin, the alleged active principle in thymus are identical to those of adenosine deaminase, it is postulated that thymosin may be a subunit of adenosine deaminase.
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PMID:A molecular hypothesis concerning the pathogenesis of myasthenia gravis. 401 May 75

The serum activities of adenosine deaminase (ADA) and its isozymes (ADA 1 and ADA 2) were measured in 31 patients with myasthenia gravis (MG). As compared with 50 normal controls, in MG the total activity and ADA 1 were significantly high (p < 0.01, respectively), and ADA 2 tended to be high. The total activity and ADA 2 were higher in generalized MG than in ocular MG. ADA 2 was significantly higher in grade IIB patients as compared with grade I patients divided by Osserman's classification (p < 0.05). Patients with bulbar signs showed a significantly high total ADA (p < 0.05) with an increasing tendency for ADA 2. There was a significant elevation of the total activity and ADA 2 in patients with positive anti-acetylcholine-receptor antibody as compared to those of the negative antibody (p < 0.05). It was concluded that total ADA, reflecting the increase of both ADA 1 and ADA 2, is high in MG; and the measurement of ADA 2 is more important because ADA 2 was increased with advancing clinical MG grade.
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PMID:Isozyme analysis of the high serum adenosine deaminase activity in patients with myasthenia gravis. 772 83

AMP dephosphorylation via ecto-5'-nucleotidase/CD73 is the rate limiting step to generate extracellular adenosine (ADO) from released adenine nucleotides. ADO, via A2A receptors (A2ARs), is a potent modulator of neuromuscular and immunological responses. The pivotal role of ecto-5'-nucleotidase/CD73, in controlling extracellular ADO formation, prompted us to investigate its role in a rat model of experimental autoimmune myasthenia gravis (EAMG). Results show that CD4(+)CD25(+)FoxP3(+) regulatory T cells express lower amounts of ecto-5'-nucleotidase/CD73 as compared to controls. Reduction of endogenous ADO formation might explain why proliferation of CD4(+) T cells failed upon blocking A2A receptors activation with ZM241385 or adenosine deaminase in EAMG animals. Deficits in ADO also contribute to neuromuscular transmission failure in EAMG rats. Rehabilitation of A2AR-mediated immune suppression and facilitation of transmitter release were observed by incubating the cells with the nucleoside precursor, AMP. These findings, together with the characteristic increase in serum adenosine deaminase activity of MG patients, strengthen our hypothesis that the adenosinergic pathway may be dysfunctional in EAMG. Given that endogenous ADO formation is balanced by ecto-5'-nucleotidase/CD73 activity and that A2ARs exert a dual role to restore use-dependent neurocompetence and immune suppression in myasthenics, we hypothesize that stimulation of the two mechanisms may have therapeutic potential in MG.
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PMID:Deficits in endogenous adenosine formation by ecto-5'-nucleotidase/CD73 impair neuromuscular transmission and immune competence in experimental autoimmune myasthenia gravis. 2569 8