Abstract: |
Background: NKT cells recognize glycolipids presented by CD1d on antigen-presenting cells (APC) and have been largely characterized by their ability to be activated by α-galactosylceramide, a glycolipid not expressed on mammalian cells. We have shown previously that GD3 can be cross-presented by CD1d to NKT cells and is the first tumor-derived glycolipid recognized by NKT cells. But the ability of NKT cells to modulate B-cell responses to tumor glycolipids that are themselves recognized by NKT cells has not been explored. Methods: We tested whether NKT cells are required for antibody (Ab) responses to GD3. We immunized wild-type mice, mice deficient in invariant chain NKT cells (iNKT cells) and mice deficient in total NKT cells against GD3. Ab titer against GD3 was measured by ELISA. Results:We found the IgM and IgG responses against GD3 were similar among the three strains of mice, including the IgG isotypes induced. Pre-expanded NKT cells to GD3 did not affect the anti-GD3 Ab response. Discussion: We conclude that Ab responses to GD3 are independent of NKT cells and that strategies to manipulate NKT cells in vivo are not likely to enhance the anti-GD3 Ab response induced by vaccines. |