Phosphatase PP2A expression levels are positively correlated to the clinical severity of systemic lupus erythematosus (SLE) and IL17A cytokine overproduction, indicating a potential role of PP2A in controlling T<sub>H</sub>17 differentiation and inflammation.
Increasing evidence supports the involvement of a catalytic subunit (PP2Ac) of protein phosphatase 2A (PP2A) in the mechanisms of systemic lupus erythematosus (SLE).
To assess the effect of increased expression of the phosphatase protein phosphatase 2A (PP2A) in T cells, as recorded in SLE patients, we generated a transgenic mouse that overexpresses the PP2Ac subunit in T cells.
Our data document increased activity of PP2A as a novel SLE disease-specific abnormality and define a distinct mechanism whereby it represses IL-2 production.