Cd55

Inhibition of immune cells Lymphocytes APC

TApoptosis ^Function

TGDIa, TFasL, TGD2 TGD2

* N.K.Cheung and W.Gerald, microarray gene expression analysis of human NB, unpublished results LMP low molecular weight protein, TAP transporter-associated protein

* N.K.Cheung and W.Gerald, microarray gene expression analysis of human NB, unpublished results LMP low molecular weight protein, TAP transporter-associated protein ing the ganglioside GD1a which is directly toxic to human lymphocytes while uncoupling cell signaling through the NFkB pathway (Shen and Ladisch 2002), as well as disialoganglioside GD2 which interferes with T-cell (Li et al. 1995) and APC functions (Shurin et al. 2001; Heitger and Ladisch 1996). Furthermore, some NB cells have been shown to express FAS-ligand (Fas-L) (Shurin et al. 1998), which may act as a death signal causing apoptosis of effector cells, such as T cells or NK cells, which themselves express the surface Fas death receptor (Takamizawa et al. 2000; Li et al. 2002). On the other hand, when confronted with antibodies, despite their low levels of CD55 (decay accelerating factor), some neuroblastomas cells have increased CD59 (homologous restriction factor) and sufficient CD46 (membrane cofactor protein) expression to render them resistant to terminal complement pathways (see 14.4.1). Effective in vivo immunotherapy must circumvent these protective mechanisms of NB in order to ultimately maximize clinical benefit.

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