miRNAs have recently emerged as key regulators of the immune system, being 
involved in lymphocyte selection and proliferation, in T(reg) cells 
differentiation, and in hematopoiesis in general. Rheumatoid arthritis (RA) is 
an autoimmune pathology the etiology of which is still obscure. Although a 
multifactorial pathogenesis has been hypothesized, the precise mechanisms 
leading to the disease are still poorly understood at the molecular level. miRNA 
expression profile analysis highlighted that miR-223 is the only miRNA that is 
strikingly deregulated in peripheral T-lymphocytes from RA patients compared 
with healthy donors. Further analysis by quantitative reverse 
transcription-polymerase chain analysis confirmed that miR-223 is overexpressed 
in T-lymphocytes from RA patients (n = 28) compared with healthy donors (n = 
10). Moreover, purification of different T-lymphocyte populations from RA 
patients highlights that miR-223 is expressed at higher levels in naive CD4(+) 
lymphocytes, whereas its expression is barely detectable in T(h)-17 cells. In 
summary, our data provide a first characterization of the miRNA expression 
profiles of peripheral T-lymphocytes of RA patients, identifying miR-223 as 
overexpressed in CD4(+) naive T-lymphocytes from these individuals. A deeper 
analysis of the biologic functions and effects of the expression of miR-223 in 
T-lymphocytes is needed to clarify the exact link between our observation and 
the disease.