Difference Between Agonist And Antagonist Muscles

The mechanism by which NO might contribute to these diseases is unknown.In addi tion to its well demonstrated cytotoxic ef fec ts, NOSZ generated NO may con tribute to neurologic disease in a subtler Benzocaine manner.Production of these soluble mediators by activated T cells, macrophages and resident glia allows for a var iety of responses including the initiation and maintenance of an inflammatory response through induction of adhesion mol ecule expression by endothelial cells, and increased expression of cytokine and chemokine receptors by infil trating cells.Furthermore, production of these factors allows for celltocell communication that might be impor tant in controlling cell proliferation, antigen presentation, and production of potentially toxic products. Both MHV and TMEV induce expression of cytokine and chemokine genes following infection of the mouse CNS.Cytokine genes that are expressed during acute MHV infec tion of the CNS include interferons alpha, beta, and gamma, interleukins alpha and beta, ILZ, IL, and IL. Furthermore, the sever ityof infection does not appear to dictate the cytokine response within the CNS.In other words, similar cytokine profiles are obtained when the highly Calcitriol neurovirulent MHVJHM or attenuated strains are used for experimental infection.Although the roleof these molecules in the pathogenesis of either the acute stage or the chronic stageof disease is unclear, it is conceivable that these mol ecules function to attract inflammatory leukocytes into the CNS following viral infection.These inflammatory leuko cy tes then contribute to host defense by eliminating virus.Mechanisms of host defense against MHV infection of the CNS include the generation of perforindependent virus specific cytotoxic T lymphocytes. Cytokines might also aid in host defense against MHV by contributing to the elimination of virus from the CNS.This is interesting in that these observations suggest separate, distinct mechanisms exist within the CNS that contribute to viral clearance.These cytokines were localized primarily to white matter tracts associated with demyelination and MHV infection, and were produced predominantly by astrocytes.The majori tyof cytokineexpressing astrocytes, however, were not infected with MHV suggesting that activation and cytokine secretion is not due to viral infection.Alternatively, these cytokines might work in concert with one another to enhance the inflammatory response, as well as to activate cells to express cytotoxic mol ecules.The chemokines CRGZIP and RANTES are expressed most abundantly in the spinal cordsof chronical ly infected mice with demyelination. Similar to what has been reported with cytokines, expression of these chemokines was localized to areasof virus persistence and demyelination.Recent reports, however, have suggested a potential role for RANTES in the pathogenesis of MS since inflammatory leukocytes have been reported to be present within MS plaque lesions.Whether RANTES has a role in contributing to virus induced demyelinating disease has yetto be determined.Studies from animal models support the idea that T cells are important contrib utors to the demyelination. For example, in the well characterized autoimmune demyelination model, EAE, demyelination has been shown to be mediated by neu roantigenspecific major histocompatibility complex have been shown to contribute to the pathogenesis of TMEV induced demyelination.Although studies have reported that T cells are essential demyelination, other work has shown that demyelination occurs when either CD or CDB T cells are depleted, however, state that their experi mental results do not exclude the possibility that T cells might be important in initiating demyelination early in the infection.

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