erratum

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Erratum (1) In this article published in the September 2011 issue of Neoplasia, the Figure 5 used was incorrect, the open and solid black triangles were erroneously switched. Shown below is the correct figure. 1. Monaco EL, Tremante E, Cerboni C, Melucci E, Sibilio L, Zingoni A, Nicotra MR, Natali PG, and Giacomini P (2011). Human leukocyte antigen E contributes to protect tumor cells from lysis by natural killer cells. Neoplasia 13: 822830. Figure 5. Block of activating receptors reveals NKG2A-mediated protection from NK lysis. The indicated tumor cell lines were tested as targets in a 51 Cr release assay using CD56 + /CD3 cells as ef- fectors, in the presence of the indicated antibodies. Blocking anti- bodies to activating receptors were selected on the basis of the ligands expressed by the target: A431 (DNAM-1), End7 (NKG2D + DNAM-1), SK-MEL 37 (DNAM-1), and Ova7 (NKG2D+DNAM-1). Dif- ferences in 51 Cr release values were statistically significant when the average values of triplicates differed from control more than three times the SD, that is, at E/T ratios from 20:1 to 2.5:1 in A431: donor 1 as well as End7:donor 1 and at E/T ratios of 20:1 and 10:1 in A431:donor 3. The top two panels display two E/T combinations in which the inhibitory effect of NKG2A becomes evident only when activating receptors are antibody-blocked. End7:donor 1 exemplifies a case in which NKG2A similarly protects in the presence and absence of antibody block. In the remaining cases, activating recep- tors and NKG2A cannot be demonstrated to influence susceptibility to lysis.

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Erratum(1) In this article published in the September 2011 issue of Neoplasia, the Figure 5 used was incorrect, the open and solid black triangles wereerroneously switched. Shown below is the correct figure.

1. Monaco EL, Tremante E, Cerboni C,Melucci E, Sibilio L, Zingoni A, Nicotra MR, Natali PG, and Giacomini P (2011). Human leukocyteantigen E contributes to protect tumor cells from lysis by natural killer cells. Neoplasia 13: 822–830.

Figure 5. Block of activating receptors reveals NKG2A-mediatedprotection from NK lysis. The indicated tumor cell lines were testedas targets in a 51Cr release assay using CD56+/CD3− cells as ef-fectors, in the presence of the indicated antibodies. Blocking anti-bodies to activating receptors were selected on the basis of theligands expressed by the target: A431 (DNAM-1), End7 (NKG2D +DNAM-1), SK-MEL 37 (DNAM-1), and Ova7 (NKG2D+DNAM-1). Dif-ferences in 51Cr release values were statistically significant whenthe average values of triplicates differed from control more thanthree times the SD, that is, at E/T ratios from 20:1 to 2.5:1 in A431:donor 1 as well as End7:donor 1 and at E/T ratios of 20:1 and 10:1 inA431:donor 3. The top two panels display two E/T combinations inwhich the inhibitory effect of NKG2A becomes evident only whenactivating receptors are antibody-blocked. End7:donor 1 exemplifiesa case in which NKG2A similarly protects in the presence andabsence of antibody block. In the remaining cases, activating recep-tors and NKG2A cannot be demonstrated to influence susceptibilityto lysis.