Murine CD4+CD25+ regulatory cells have been reported to express latency-associated peptide (LAP) and TGF-β on the surface after activation, and exert regulatory function by the membrane-bound TGF-β in vitro. We have now found that a small population of CD4+ T cells, both CD25+ and CD25−, can be stained with a goat anti-LAP polyclonal Ab without being stimulated. Virtually all these LAP+ cells are also positive for thrombospondin, which has the ability to convert latent TGF-β to the active form. In the CD4+CD45RBhigh-induced colitis model of SCID mice, regulatory activity was exhibited not only by CD25+LAP+ and CD25+LAP− cells, but also by CD25−LAP+ cells. CD4+CD25−LAP+ T cells were part of the CD45RBlow cell fraction. CD4+CD25−LAP−CD45RBlow cells had minimal, if any, regulatory activity in the colitis model. The regulatory function of CD25−LAP+ cells was abrogated in vivo by anti-TGF-β mAb. These results identify a new TGF-β-dependent regulatory CD4+ T cell phenotype that is CD25− and LAP+.

Bacterial canker of Kiwifruit (Actinidia chinensis) has recently been reported in Japan. The causal pathogen is classified in Pseudomonas syringae on the basis of laboratory tests and is similar to, but not identical with, P. syringae pv. morsprunorum. In inoculated kiwifruit, the pathogen from kiwifruit reproduces the characteristic canker and leaf spot symptoms.P. syringae pv. syringae and P. syringae pv. morsprunorum are only weakly virulent to kiwifruit.The pathogen from kiwifruit is weakly pathogenic to peach and Japanese apricot, but not to 24 other plant species tested. The pathogen is considered to be a pathovar of P. syringae and the name P. syringae pv. actinidiae pv. nov. is proposed. Strain Kw-11 (ICMP9617) is designated as the pathotype strain.

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