The Rise and Fall of the So-Called Chronicler’s History and the Current Study of the Composition of Chronicles, Ezra, and Nehemiah

While the books of Chronicles, Ezra, and Nehemiah share many themes and vocabulary, they do not come from one author, and the Chronicler’s History hypothesis cannot be supported. Discussions about different Hebrew vocabulary in these books have not been conclusive. The apocryphal book of 1 Esdras does not support the Chronicler’s History hypothesis because it is a secondary rearrangement of Chronicles, Ezra, and Nehemiah plus an additional story about the three guardsmen, which provides an appropriate introduction to Zerubbabel, a leader in the postexilic community. A number of theological/ideological differences show that Chronicles, Ezra, and Nehemiah did not come from a single author: differences about mixed marriages, the history of early Israel; the positive attitude toward the north in Chronicles. The books of 1 and 2 Chronicles give more significance to David than Ezra and Nehemiah do. But these three books advocate for the primacy of Jerusalem, the exclusive status of the Jerusalem temple, and the importance of the priests and Levites.

A Role for Interferon Regulatory Factor 4 in Receptor Editing

ABSTRACT Receptor editing is the primary means through which B cells revise antigen receptors and maintain central tolerance. Previous studies have demonstrated that interferon regulatory factor 4 (IRF-4) and IRF-8 promote immunoglobulin light-chain rearrangement and transcription at the pre-B stage. Here, the roles of IRF-4 and -8 in receptor editing were analyzed. Our results show that secondary rearrangement was impaired in IRF-4 but not IRF-8 mutant mice, suggesting that receptor editing is defective in the absence of IRF-4. The role of IRF-4 in receptor editing was further examined in B-cell-receptor (BCR) transgenic mice. Our results show that secondary rearrangement triggered by membrane-bound antigen was defective in the IRF-4-deficient mice. Our results further reveal that the defect in secondary rearrangement is more severe at the immunoglobulin λ locus than at the κ locus, indicating that IRF-4 is more critical for the λ rearrangement. We provide evidence demonstrating that the expression of IRF-4 in immature B cells is rapidly induced by self-antigen and that the reconstitution of IRF-4 expression in the IRF-4 mutant immature B cells promotes secondary rearrangement. Thus, our studies identify IRF-4 as a nuclear effector of a BCR signaling pathway that promotes secondary rearrangement at the immature B-cell stage.