RESUMEN
In patients with prevalent psoriasis a positive influence amino acid addition (with the standart therapy) on the clinical status of patients and their immune status induces. As a result of this addition use the lesion area diminished, prolongation of remission periods, reduction of the time spent in hospital.
Asunto(s)
Aminoácidos/uso terapéutico , Psoriasis/dietoterapia , Psoriasis/inmunología , Adenosina Trifosfatasas/sangre , Adenosina Trifosfatasas/efectos de los fármacos , Adulto , Antígenos CD/sangre , Antígenos CD/efectos de los fármacos , Antígenos de Diferenciación de Linfocitos B/sangre , Antígenos de Diferenciación de Linfocitos B/efectos de los fármacos , Apirasa , Linfocitos B/efectos de los fármacos , Linfocitos B/inmunología , Dieta , Suplementos Dietéticos , Humanos , Persona de Mediana Edad , Psoriasis/patología , Receptores de Interleucina-2/sangre , Receptores de Interleucina-2/efectos de los fármacos , Receptores de Transferrina , Receptor fas/sangre , Receptor fas/efectos de los fármacosRESUMEN
In RBL-2H3 rat leukemic mast cells, cross-linking anti-DNP IgE-receptor complexes with multivalent antigen (DNP-BSA) activates a signal transduction pathway leading to Ca2+ influx and secretion. Cross-linking IgE-receptor complexes also stimulates a pathway that inactivates (desensitizes) receptors; this pathway becomes important at high concentrations of cross-linking antigen. Recent evidence that antigen-induced secretion is impaired by mycophenolic acid (MPA), an inhibitor of guanine nucleotide synthesis de novo, has implicated a GTP-binding protein (G protein) in the signaling pathway. Other recent studies have indicated that the conversion of cross-linked receptors to a detergent-insoluble (cytoskeleton-associated) form at high antigen concentrations is correlated with the loss of signaling activity. Here we show that secretion elicited by an optimal concentration of antigen (0.05 micrograms/ml DNP-BSA) is only inhibited by about 25% in guanine nucleotide-depleted cells, whereas secretion elicited by 5 micrograms/ml DNP-BSA, a concentration in the range that causes the high-dose inhibition of secretion, is inhibited by more than 60%. We also show that IgE-receptor complexes are insolubilized in response to 5 but not 0.05 micrograms/ml DNP-BSA in both control and guanine nucleotide-depleted cells. Importantly, the extent of insolubilization elicited by 5 micrograms/ml DNP-BSA is increased by more than 60% in the guanine nucleotide-depleted samples. These results raise the possibility that guanine nucleotide depletion reduces the secretory response to high antigen concentrations in two ways: by inhibiting the G protein-coupled signaling pathway and by increasing the availability of receptors to the pathway leading to receptor insolubilization and inactivation.