Fig. 6

Anti-nociceptive T cell activity is mediated by enkephalins in mice. a Splenocytes from PENK^+/+ wild-type C57Bl/6 (circle) or PENK^−/− pre-proenkephalin knockout (triangle) mice were transferred i.v. into immune-deficient RAG-2^−/− mice (n = 12 for each group of mice). The next day, mice were immunized s.c. into hind footpads with OVA in CFA. Immunized non-transferred RAG2^−/− mice (n = 10, diamond) were used as control. Inflammatory pain was monitored by measuring sensitivity of the mice to mechanical stimuli using the von Frey test. Data are expressed as mean ± SEM paw withdrawal thresholds measured in inflamed ipsilateral immunized paws (open symbol) and contralateral non-injected paws (closed symbol). Results were obtained from two sets of experiments performed on groups of six (T cell transferred) or five (RAG2^−/−) mice. ***p < 0.001 (comparison with immunized non-transferred RAG-2^−/− mice). b From day 3 until the end of the experiment, recipient RAG2^−/− mice transferred with either PENK^+/+ (square; n = 6) or PENK^−/− (inverted triangle; n = 6) splenocytes were daily injected into inflamed hind paw with 10 μL of naloxone methiodide (NLX-Meth) at 2 mg mL⁻¹, 30 min before pain assessment. Mice were randomly assigned into each group in blind experiments in which the treatment and pain assessment were performed by two different experimenters. Data are expressed as mean ± SEM paw withdrawal thresholds measured in inflamed ipsilateral immunized paws (open symbol) and contralateral non-injected paws (closed symbol). Results were obtained from two sets of experiments performed on groups of mice mice