To this end, CD4+ T cells may acquire proinflammatory phenotypes, such as T helper (Th) 1 and Th17, as well as anti-inflammatory phenotypes, such as Th2 and the T regulatory (Treg) 1 [20, 21], and evidence from animal models of PD suggests that Th1 and Th17 may be detrimental while Th2 and Treg may be protective (reviewed in [22]). The gene discussed is CD4; the disease is Parkinson disease.