In this article, the controversial role of @entity842 (NO) in T helper (Th) cell activation and T-cell-dependent immunity will be discussed with an emphasis on immunosuppression by NO. NO is generated by @entity1358 ( @entity1358 ) during the process of antigen presentation to T cells. In @entity19 models, activation of the @entity13633 ( @entity13633 ) in @entity1358 is triggered by Th1-cell-derived @entity60 , in combination with other soluble or membrane-associated T-cell factors. The NO so-produced inhibits T-cell proliferation, while it does not inhibit T cell cytokine production. NO blocks T-cell proliferation during G1/S transition. In @entity19 models of T-cell-mediated autoimmunity such as myelin antigen-induced EAE, the disease is exacerbated by genetic deletion of @entity13633 , indicating that NO suppresses T-cell-mediated immunity in vivo. Recent studies reveal that interaction with @entity224 diminishes the T-cell regulatory activity of NO. The role for @entity1110 oxidase as a source for NO-inhibiting @entity224 is discussed. In conclusion, NO plays an important regulatory role in the induction phase of T-cell-mediated immunity. @entity224 may enhance T-cell-mediated immunity by preventing the immunosuppressive activity of NO.

XXXX and T helper cell immunity.

@entity19 :: ('10090', 'Species') :: ['mouse'] @entity60 :: ('15978(Tax:10090)', 'Gene') :: ['IFN-gamma'] @entity1110 :: ('MESH:D009249', 'Chemical') :: ['NADPH'] @entity1358 :: ('MESH:D002292', 'Disease') :: ['APC', 'antigen-presenting cells'] @entity842 :: ('MESH:D009569', 'Chemical') :: ['nitric oxide'] @entity13633 :: ('18126(Tax:10090)', 'Gene') :: ['inducible NO synthase', 'iNOS'] @entity224 :: ('MESH:D013481', 'Chemical') :: ['superoxide', 'Superoxide']
@entity842 :: (MESH:D009569,Chemical) :: ['Nitric oxide']
