FcγRIII engagement provides activating signals to NKT cells in antibody-induced joint inflammation
J. Clin. Invest. Hye Young Kim, et al. 116:2484
doi:10.1172/JCI27219 [Go to this article.]

Figure 3
Adoptive transfer of Fc γR–/– mouse NKT cells into CD1d–/– mice does not restore joint inflammation in a K/BxN serum transfer model. (A) Sorted NKT cells (3 × 105 cells/mouse) from B6 or FcγR–/– mice were adoptively transferred into CD1d–/– mice (B6 NKT transfer or FcγR–/– NKT transfer, respectively) 1 day before the K/BxN serum transfer (n = 5 per group). Clinical scores and ankle thickness were monitored in B6 and CD1d–/– mice as well as in CD1d–/– mice administered NKT cells of B6 or FcγR–/– mice after injecting K/BxN serum. (B) Histological and gross examination of the ankle joints of B6 and CD1d–/– mice as well as CD1d–/– mice administered B6 or FcγR–/– mouse NKT cells 5 days after serum transfer. Original magnification, ×200 (middle panels); ×1,000 (bottom panels). Arrows in bottom panels indicate neutrophils in the joint tissues. (C) RT-PCR and real-time PCR were used to determine Vα14Jα218 TCR mRNA levels in the ankle joint tissues of B6 and CD1d–/– mice as well as CD1d–/– mice administered B6 or FcγR–/– mouse NKT cells. RT-PCR and real-time PCR were performed 10 days after K/BxN serum transfer. (D) TGF-β1, IL-4, and IFN-γ mRNA levels were measured by real-time PCR in the joint tissues and spleens of B6 mice, CD1d–/– mice, and CD1d–/– mice administered B6 or FcγR–/– mouse NKT cells 10 days after K/BxN serum transfer. Results are representative of 3 independent experiments. *P < 0.05; **P < 0.01.