Table 1.
Cell Type | Effect of ASM | References |
---|---|---|
Macrophages | Induces/amplifies inflammatory signals with cytokine production. Promotes proper fusion of late phagosomes with lysosomes. Promotes macrophage apoptosis. |
[34,35,36,37,38], [41] |
NK Cells | Influences these cells function via CD161. Leads to activation of NK cell signaling pathways. Is involved in NK cell apoptosis. |
[45,46] |
B Cells | Mediates CD40 clustering and in this way mediates B cell activation. Is involved with plasma membrane damage repair. Important for autophagic function. |
[48,51], [52,53] |
CD4+ T Cells | Involved in TCR mediated activation. Involved with polarization into subtypes Th1, Th2 and Th17. Acts a negative regulator of Tregs. |
[54,58,59,60], [62] |
CD8+ T Cells | Involved in the cellular membrane’s biophysical properties inducing the extrusion of lytic granules from the cells by promoting secretory granules contraction. | [64] |
iNKT Cells | Involved in iNKT cell development and activation. ASM substrate sphingomyelin impedes CD1d access to antigenic lipids, thus reducing iNKT activation. |
[33] |