Abstract:
:Whilst many physiological functions of nitric oxide (NO) have been revealed so far, recent evidence proposes an essential role for NO in T lymphocyte activation and signal transduction. NO acts as a second messenger, activating soluble guanyl cyclase and participating in signal transduction pathways involving cyclic GMP. NO modulates mitochondrial events that are involved in apoptosis and regulates mitochondrial biogenesis in many cell types, including lymphocytes. Several studies undertaken on patients with RA and SLE have documented increased endogenous NO synthesis, although the effects of NO may be distinct. Here, we discuss recent evidence that NO contributes to T cell dysfunction in both SLE and RA by altering multiple signaling pathways in T cells. Although NO may play a physiological role in lymphocyte cell signaling, its overproduction may perturb T cell activation, differentiation and effector responses, each of which may contribute in different ways to the pathogenesis of autoimmunity.
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Nagy G,Clark JM,Buzás EI,Gorman CL,Cope APdoi
10.1016/j.imlet.2007.04.013subject
Has Abstractpub_date
2007-07-31 00:00:00pages
1-5issue
1eissn
0165-2478issn
1879-0542pii
S0165-2478(07)00104-6journal_volume
111pub_type
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