Antibody function

Antibody catalysis of the oxidation of water.

Wentworth, P. Jr et al. Science 293, 1806?1811 (2001)

It was recently shown that antibodies can generate hydrogen peroxide from singlet oxygen. The authors now show that the oxidation of water serves as the electron source for this catalytic process. They also identified a highly conserved oxygen-binding domain within the immunological fold in which this unusual chemistry might take place. Whether this reaction allows antibodies to detoxify singlet oxygen, or aids in cell killing through the production of hydrogen peroxide, remains to be determined.

Regulatory T cells

Cell contact-dependent immunosuppression by CD4 + CD25 + regulatory T cells is mediated by cell surface-bound transforming growth factor-β.

Nakamura, K., Kitani, A. & Strober, W. J. Exp. Med. 194, 629?644 (2001)

CD4+CD25+ regulatory T cells mediate suppression of CD4+CD25− T cells in a cell-contact-dependent manner, and in the absence of secreted cytokines. Nakamura and colleagues show that these cells do, in fact, produce the suppressive cytokines transforming growth factor-β (TGFβ) and interleukin-10, and that suppression is dependent on presentation of TGFβ at the cell surface.

Haematopoiesis

The Notch ligand, Delta-1, inhibits the differentiation of monocytes into macrophages but permits their differentiation into dendritic cells.

Ohishi, K. et al. Blood 98, 1402?1407 (2001)

Notch signalling pathways regulate cell-fate decisions in many developmental systems. The authors studied the role of the Notch ligand, Delta-1, in monocyte differentiation. Monocytes cultured in the presence of the immobilized extracellular domain of Delta 1 (Deltaext-myc) and appropriate cytokines can differentiate into mature dendritic cells (DCs) but not into macrophages. The results indicate a role for Notch signalling in the regulation of cell-fate decisions by bipotent macrophage/DC precursors.

T-cell development

Early thymocyte development is regulated by modulation of E2A protein activity

Engel, I. et al. J. Exp. Med 194, 733?746 (2001)

The products of the E2A gene (the E47 and E12 basic HLH transcription factors) are important in T-cell development. Here, the authors show that the block in T-cell development seen in Rag−/− and scid mutant mice can be rescued by a deficiency in E2A. In addition, mimicing pre-TCR signals in Rag−/− thymocytes resulted in decreased E47 DNA-binding and increased expression of the E-protein antagonist Id3. They conclude that E2A acts to ensure the developmental arrest of thymocytes with defects in TCRβ expression.