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.