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Invariant natural killer T cells (iNKT) produce large amounts of different cytokines which can influence differentiation, polarization and activation of immune cells, particularly NK and T cells. iNKT have been shown to suppress GvHD and promote anti-tumor and anti-pathogen immunity. There are highly specific and safe synthetic ligands such as alpha-galactosylceramide (α-GalCer) and C20:2 which activate iNKT cells toward relatively Th1 and Th2 pathways, respectively. Bone marrow transplantation (BMT) or 'hematopoietic stem cell transplantation' (HSCT) is effective for leukemia and lymphoma through 'graft-versus-leukemia' (GVL) immunity. However, frequent serious complications include graft-versus-host-disease (GVHD), opportunistic infections and relapse. Both GVHD and GVL are mediated by T cells. Manipulating iNKT by different lipid analogues in early and late phases after transplantation may suppress GVHD and graft rejection and enhance GVL effect, as well as resistance to opportunistic infections and so, could be a novel and effective strategy for improving HSCT outcome.

Nasal polyps (NP) are associated with inflamed mucosa of unknown etiology. The role of T cells in nasal polyposis is unclear. Invariant natural killer T cells (iNKT) can promote Th2 responses and have been implicated in some types of asthma. As there are shared inflammatory pathways involved in asthma and NPs, we evaluated the frequency of iNKT in 17 patients with NPs, but without asthma. A median of 6% polyp cells were T lymphocytes, of which iNKT were 0 to 2.38% (mean 0.674%). In the matched group (n = 10), iNKT in NPs was significantly higher than PBMCs (1.057% vs 0.155%, P 0.05). Relative expression of Vα24 to TCR-beta genes in polyps (n = 14) was higher than blood in matched samples (n = 4). The presence of greater proportions of iNKT in NPs than in blood suggests that iNKT may play a role in the pathogenesis of nasal polyposis.