A. Bussing et al., SELECTIVE KILLING OF CD8(-ACETYL-D-GALACTOSAMINE-SPECIFIC LECTIN FROMVISCUM-ALBUM L() CELLS WITH A MEMORY PHENOTYPE (CD62L(LO)) BY THE N), Cell death and differentiation, 5(3), 1998, pp. 231-240
As reported previously by our group, among the toxic proteins from Vis
cum album L. only the mistletoe lectins (MLs) induce the apoptotic kil
ling pathway in human lymphocytes, Although one may expect a homogenou
s distribution of carbohydrate domains on cell surface receptors for t
he carbohydrate binding B chains of the toxic protein, the sensitivity
of cells to these B chains obviously differ. Here we report a selecti
ve killing of CD8(+) CD62L(lo) cells from healthy individuals by the g
alNAc-specific ML III (and RCA(60) which binds to gal and galNAc), whi
le the gal-specific ML I was less effective. This selective killing is
not sufficiently explained by protein synthesis inhibition alone, sin
ce this subset was not affected by other ribosome inhibiting proteins
such as the lectin from Ricinus communis (RCA(120)), lectin from Abrus
precatorus (APA), abrin A, and inhibitors of RNA, DNA and/or protein
synthesis such as actinomycin D, mitomycin C, and cycloheximide, We co
nclude that CD8(+) cells with 'memory' phenotype (CD62L(lo)) are more
sensitive to the ML III-mediated killing than their CD8(+) CD62L(hi) c
ounterparts, CD4(+) T cells, and CD19(+) B cells, These cells probably
express a distinct receptor with galNAc domains that is missing or no
t active on CD8(+) cells with a 'naive' phenotype.