Effects of temperature and wetness duration on conidial infection, latent period and asexual sporulation of Pyrenopeziza brassicae on leaves of oilseed rape

Experiments in controlled environments were carried out to determine the effects of temperature and leaf wetness duration on infection of oilseed rape leaves by conidia of the light leaf spot pathogen, Pyrenopeziza brassicae . Visible spore pustules developed on leaves of cv. Bristol inoculated with P. brassicae conidia at temperatures from 4 to 20°C, but not at 24°C; spore pustules developed when the leaf wetness duration after inoculation was longer than or equal to approximately 6 h at 12–20°C, 10 h at 8°C, 16 h at 6°C or 24 h at 4°C. On leaves of cvs. Capricorn or Cobra, light leaf spot symptoms developed at 8 and 16°C when the leaf wetness duration after inoculation was greater than 3 or 24 h, respectively. The latent period (the time period from inoculation to first spore pustules) of P. brassicae on cv. Bristol was, on average, approximately 10 days at 16°C when leaf wetness duration was 24 h, and increased to approximately 12 days as temperature increased to 20°C and to 26 days as temperature decreased to 4°C. At 8°C, an increase in leaf wetness duration from 10 to 72 h decreased the latent period from approximately 25 to 16 days; at 6°C, an increase in leaf wetness duration from 16 to 72 h decreased the latent period from approximately 23 to 17 days. The numbers of conidia produced were greatest at 12–16°C, and decreased as temperature decreased to 8°C or increased to 20°C. At temperatures from 8 to 20°C, an increase in leaf wetness duration from 6 to 24 h increased the production of conidia. There were linear relationships between the number of conidia produced on a leaf and the proportion of the leaf area covered by 'lesions' (both log₁₀-transformed) at different temperatures.     

Trans-endocytosis of CD80 and CD86: a molecular basis for the cell-extrinsic function of CTLA-4

Cytotoxic T lymphocyte antigen 4 (CTLA-4) is an essential negative regulator of T cell immune responses whose mechanism of action is the subject of debate. CTLA-4 shares two ligands (CD80 and CD86) with a stimulatory receptor, CD28. Here, we show that CTLA-4 can capture its ligands from opposing cells by a process of trans-endocytosis. After removal, these costimulatory ligands are degraded inside CTLA-4-expressing cells, resulting in impaired costimulation via CD28. Acquisition of CD86 from antigen-presenting cells is stimulated by T cell receptor engagement and observed in vitro and in vivo. These data reveal a mechanism of immune regulation in which CTLA-4 acts as an effector molecule to inhibit CD28 costimulation by the cell-extrinsic depletion of ligands, accounting for many of the known features of the CD28-CTLA-4 system.