Synergy between the light-induced acute response and the circadian cycle: a new mechanism for the synchronization of the Phaseolus vulgaris clock to light

PvLHY and Lhcb expression has been studied in primary bean leaves after exposure of etiolated leaves to two or three white light-pulses and under different photoperiods. Under the tested photoperiods, the steady-state mRNA levels exhibit diurnal oscillations with zenith in the morning between ZT21 and 4 for PvLHY and between ZT4 and 6 for Lhcb. Nadir is in the evening between ZT12 and 18 for PvLHY and ZT18 and 24 for Lhcb. Light-pulses to etiolated seedlings induce a differentiated acute response that is reciprocally correlated with the amplitude of the following circadian cycle. In addition, the clock modulates the duration of the acute response (descending part of the curve included), which according to the phase of the rhythm at light application extends from 7 to 18 h. This constitutes the response dynamics of the Phaseolus clock to light. Similarly, the waveform of PvLHY and Lhcb expression during the day of different photoperiods resembles in induction capability (accomplishment of peak after lights-on) and duration (from lights-on phase to trough) the phase-dependent progression of acute response in etiolated seedlings. Consequently, the peak of Lhcb (all tested photoperiods) and PvLHY (in LD 18:6) attained in the photophase corresponds to the acute response peak, while the peak of PvLHY during the scotophase (in LD 12:12 and 6:18) corresponds to the circadian peak. Thus, the effect of the response dynamics in the photoperiod determines the coincidence of the peak with the photo- or scotophase, respectively. This represents a new model mechanism for the adaptation of the Phaseolus clock to light.     

Modeling the role of IL-2 in the interplay between CD4+ helper and regulatory T cells: Assessing general dynamical properties

Mathematical models accounting for well-known evidences relating to the dynamics of interleukin 2, helper and regulatory T cells are presented. These models extend an existent model (the so-called cross-regulation model of immunity), by assuming IL-2 as the growth factor produced by helper cells, but used by both helper and regulatory cells to proliferate and survive. Two model variants, motivated by current literature, are explored. The first variant assumes that regulatory cells suppress helper cells by limiting IL-2 production and consuming the available IL-2; i.e. they just trigger competition for IL-2. The second model variant adds to the latter competitive mechanism the direct inhibition of helper cells activation by regulatory cells. The extended models retain key dynamical features of the cross-regulation model. But such reasonable behavior depends on parameter constraints, which happen to be realistic and lead to interesting biological discussions. Furthermore, the introduction of IL-2 in these models breaks the local/specific character of interactions, providing new properties to them. In the extended models, but not in the cross-regulation model, the response triggered by an antigen affects the response to other antigens in the same lymph node. The first model variant predicts an unrealistic coupling of the immune reactions to all the antigens in the lymph node. In contrast, the second model variant allows the coexistent of concomitant tolerant and immune responses to different antigens. The IL-2 derived from an ongoing immune reaction reinforces tolerance to other antigens in the same lymph node. Overall the models introduced here are useful extensions of the cross-regulation formalism. In particular, they might allow future studies of the effect of different IL-2 modulation therapies on CD4+ T cell dynamics.