Table 1 |
||
|
Nitric oxide-induced T cell functions in sysemic lupus erythematosus and rheumatoid arthritis |
||
|
Altered T cell function |
SLE |
RA |
|
|
||
|
Mitochondrial hyperpolarization and biogenesis |
Higher [10] |
Normal [27] |
|
Tlymphocyte NO production |
Normal [10] |
Increased [27] |
|
TCR-induced rapid and sustained Ca2+ signal |
Rapid-increased, sustained-decreased [10] |
Normal [22] |
|
TCR expression |
Decreased [34] |
Decreased [61] |
|
mTOR activity |
Increased [29] |
Not known |
|
ATP level |
Decreased [28] |
Normal [28] |
|
Monocyte NO production |
Increased [10] |
Increased [46] |
|
|
||
|
mTOR, mammalian target of rapamycin; NO, nitric oxide; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; TCR, T cell antigen receptor. |
||
|
Nagy et al. Arthritis Research & Therapy 2010 12:210 doi:10.1186/ar3045 |
||