[Cytokines and the nervous system: the relationship between seizures and epilepsy]. / Citocinas y sistema nervioso: relacion con crisis convulsivas y epilepsia.

INTRODUCTION. The immune system and the peripheral and central nervous system are in constant communication by means of messengers and signalling molecules released, such as cytokines, neuropeptides, neurohormones and neurotransmitters, among others. Seizures are defined as the transitory appearance of signs and symptoms that trigger an abnormally excessive neuronal activity in the brain. Following seizures the generation of a neuroinflammatory process has been observed to occur, with the consequent release of proinflammatory cytokines and inflammation-mediating molecules, which make the patient more prone to epilepsy. AIM. To offer evidence suggesting and supporting the role of cytokines in the appearance of seizures and in epilepsy, since these molecules have proven to have dual properties. DEVELOPMENT. The central nervous system, by means of the blood-brain barrier, restricts the flow of activated cells and inflammation mediators released from the peripheral system towards the brain parenchyma. Moreover, there is also another series of mechanisms that contributes to the 'selective and modified' immunity of the central nervous system. The purpose of all this series of events is to limit the responses of the immune system at central level, although it has been shown that in the central nervous system they are permanently under the control and regulation of the immune system. CONCLUSIONS. Cytokines in epilepsy play a dual role with pro- and anti-convulsive properties. Seizures do not induce the expression of cytokines only inside the brain, but also peripherally.

TITLE: Citocinas y sistema nervioso: relacion con crisis convulsivas y epilepsia.Introduccion. El sistema inmune y el sistema nervioso periferico y central se encuentran en constante comunicacion a traves de mensajeros y moleculas de señalizacion liberadas, como las citocinas, los neuropeptidos, las neurohormonas y los neurotransmisores, entre otros. Las convulsiones se definen como la aparicion transitoria de signos y sintomas que inducen una actividad neuronal excesiva anormal en el cerebro; despues de una crisis convulsiva, se ha observado la generacion de un proceso neuroinflamatorio, con la consecuente liberacion de citocinas proinflamatorias y de moleculas mediadoras de inflamacion, que predisponen a la epilepsia. Objetivo. Mostrar la evidencia que sugiere y apoya el papel de las citocinas en la aparicion de crisis convulsivas y en la epilepsia, ya que estas moleculas han demostrado propiedades duales. Desarrollo. El sistema nervioso central, a traves de la barrera hematoencefalica, restringe el flujo de celulas activadas y de mediadores de inflamacion liberados desde el sistema periferico hacia el parenquima cerebral; ademas, existe otra serie de mecanismos que contribuyen a la inmunidad 'selectiva y modificada' del sistema nervioso central. Toda esta serie de eventos tiene la finalidad de limitar respuestas del sistema inmune a nivel central, aunque se ha demostrado que en el sistema nervioso central se encuentran de manera permanente bajo el control y la regulacion del sistema inmune. Conclusiones. Las citocinas en la epilepsia muestran un papel dual con propiedades pro y anticonvulsionantes. Las convulsiones no solamente inducen la expresion de citocinas dentro del cerebro, sino tambien perifericamente.

Associations of killer cell immunoglobulin- like receptor genes with rheumatoid arthritis.

OBJECTIVE: Rheumatoid Arthritis (RA) is an autoimmune and chronic inflammatory disease of unknown etiology. Killer cell immunoglobulin-like receptors are expressed on the surface of natural killer cells and CD28null T-cells, both present in synovial membrane of RA. Therefore we evaluated the associations of KIR genes with RA. METHODS: 16 KIR genes were genotyped in 100 healthy subjects (HS) and 100 RA patients from Western Mexico using PCR-SSP. Differences in KIR genotypes and gene frequencies were assessed using the X^{2} test. RESULTS: Gene frequency of KIR2DL3 was lower in RA than in HS (p= 0.0019), whereas KIR2DL2 and KIR2DS2 were higher in RA than HS (p =0.0004 and p = 0.0487, respectively). In addition were identified 38 genotypes (from G1-G38) in both studied groups, and the genotype frequencies of G1, G6 and G14 showed significant differences (p =0.0001, p =0.0208 and p =0.0300, respectively). CONCLUSIONS: The presence of KIR2DL2, KIR2DS2 and absence of KIR2DL3 are associated with RA. Moreover, two genotypes BX are associated with RA. These results suggest that KIRs can be involved in RA susceptibility.