A catastrophic consequence of peripheral nerve injury is the development of 
abnormal, chronic neuropathic pain. The inflammatory response at the injury site 
is believed to contribute to the generation and maintenance of such persistent 
pain. However, the physiological significance and potential contribution of T 
cells to neuropathic pain remains unclear. Here we show that T cells infiltrate 
injured sciatic nerves following chronic constriction injury (CCI), but not 
uninjured nerves. Congenitally athymic nude rats, which lack mature T cells, 
developed a significantly reduced mechanical allodynia and thermal hyperalgesia 
following CCI, compared with their heterozygous littermates. To understand 
further the role played by different T-cell subsets, we generated polarized 
populations of type 1 and type 2 T cells, with different cytokine secretion 
profiles, from spleens of sciatic nerve-injured heterozygous rats. Passive 
transfer of type 1 T cells, which produce proinflammatory cytokines, into nude 
rats enhanced the recipients' pain hypersensitivity to a level similar to that 
of heterozygous donor rats. In contrast, passive transfer of polarized type 2 T 
cells, which produce anti-inflammatory cytokines, into heterozygous rats 
modestly though significantly attenuated their pain hypersensitivity. Thus, 
injection of type 1 and type 2 T-cell subsets produces opposing effects on 
neuropathic pain. These findings suggest the modulation of the T-cell immune 
response as a potential target for the treatment of neuropathic pain.