Högerkorp, C.-M., and C. A. K. Borrebaeck. 2006. The human CD77− B cell population represents a heterogeneous subset of cells comprising centroblasts, centrocytes, and plasmablasts, prompting phenotypical revision. J. Immunol. 177: 4341–4349.
In Results, under the heading Phenotypic B cell markers correspond to mRNA expression, in the second paragraph, sentence four, the designation “B cell line (BCL)6” is incorrect. The corrected sentence is shown below.
As expected, BCL6 was found to be typically linked to GC B cell subsets accompanied by a strong down-regulation of BCL2 (Fig. 4A).
Under the heading CD77− cells share the CD77− cell proliferation program, in sentence four, six, and seven, cyclin D3, E1, E2, A2, B1, B2, p27Kip, p18, and BMI1 should be italicized. The corrected sentences are shown below.
Genes, including cyclin D3 (CCND3), E1 (CCNE1), E2 (CCNE2), A2 (CCNA2), B1 (CCNB1), and B2 (CCNB2), all regulators of the G1-S, S, and G2-M phase transitions, were expressed in both of these subsets… . Furthermore, the inhibitors of CDK2, p21Cip (CDKN1A) and p27Kip (CDKN1B), were effectively down-regulated, and among the inhibitors of CDK4 class of proteins (INK4) only p18 (CDKN2C) displayed an increased expression in the GC B cell subsets. The members of the polycomb group of genes, ENX and EED, involved in proliferation (12) were also highly up-regulated in the GC B subsets, whereas BMI1 was equally significantly down-regulated (Fig. 4C) in both subsets (13).
Under the heading The GC genomic integrity and DNA maintenance programs are active in both the CD77− and CD77− population, in sentence five, p53 (TP53) should be italicized.
Notable was that p53 (TP53), another target of ATM, displayed a baseline expression pattern across all B cell subsets.
Under the heading Transcriptional regulation of SHM and CSR does not separate CD77− and CD77−, in the first paragraph, sentence five, “MutS homologue 2 (MSH2), MutS homologue 6 (MSH6)” are incorrect; and EXO1 and UNG should be italicized. In the first sentence of the third paragraph, H2AX, XRCC4 DDB2, and XPG should be italicized. The corrected sentences are shown below.
This transcriptional regulation was seen also among components participating in MMR, such as the MSH2, MSH6, and EXO1 (Fig. 6C), as well as for the BER enzyme UNG (Fig. 6D), which is noteworthy considering the specific implication of these particular MMR and BER members in SHM (19).
As for the regulation of the repair pathways implicated in CSR, the nonhomologous end joining members H2AX (H2AFX) and DNA-PKcs (PRKDC) (14) together with XRCC4 demonstrated an activation-induced expression seen in both GC B cell subsets (Fig. 6G), and the only members of the nucleotide excision repair pathway that changed were the DDB2, which increased, and the XPG (ERCC5), which surprisingly decreased in the GC subsets (Fig. 6E).
- Copyright © 2006 by The American Association of Immunologists