No abstract

The objective of the present study was to compare a random regression model, usually used in genetic analyses of longitudinal data, with the structured antedependence (SAD) model to study the longitudinal feed conversion ratio (FCR) in growing Large White pigs and to propose criteria for animal selection when used for genetic evaluation. The study was based on data from 11,790 weekly FCR measures collected on 1,186 Large White male growing pigs. Random regression (RR) using orthogonal polynomial Legendre and SAD models was used to estimate genetic parameters and predict FCR-based EBV for each of the 10 wk of the test. The results demonstrated that the best SAD model (1 order of antedependence of degree 2 and a polynomial of degree 2 for the innovation variance for the genetic and permanent environmental effects, i.e., 12 parameters) provided a better fit for the data than RR with a quadratic function for the genetic and permanent environmental effects (13 parameters), with Bayesian information criteria values of -10,060 and -9,838, respectively. Heritabilities with the SAD model were higher than those of RR over the first 7 wk of the test. Genetic correlations between weeks were higher than 0.68 for short intervals between weeks and decreased to 0.08 for the SAD model and -0.39 for RR for the longest intervals. These differences in genetic parameters showed that, contrary to the RR approach, the SAD model does not suffer from border effect problems and can handle genetic correlations that tend to 0. Summarized breeding values were proposed for each approach as linear combinations of the individual weekly EBV weighted by the coefficients of the first or second eigenvector computed from the genetic covariance matrix of the additive genetic effects. These summarized breeding values isolated EBV trajectories over time, capturing either the average general value or the slope of the trajectory. Finally, applying the SAD model over a reduced period of time suggested that similar selection choices would result from the use of the records from the first 8 wk of the test. To conclude, the SAD model performed well for the genetic evaluation of longitudinal phenotypes.

NK cells utilize a large array of receptors to screen their surroundings for aberrant or virus‐infected cells. Given the vast diversity of receptors expressed on NK cells we seek to identify receptors involved in the recognition of HIV‐1‐infected cells. By combining an unbiased large‐scale screening approach with a functional assay, we identify TRAIL to be associated with NK cell degranulation against HIV‐1‐infected target cells. Further investigating the underlying mechanisms, we demonstrate that TRAIL is able to elicit multiple effector functions in human NK cells independent of receptor‐mediated induction of apoptosis. Direct engagement of TRAIL not only results in degranulation but also IFNγ production. Moreover, TRAIL‐mediated NK cell activation is not limited to its cognate death receptors but also decoy receptor I, adding a new perspective to the perceived regulatory role of decoy receptors in TRAIL‐mediated cytotoxicity. Based on these findings, we propose that TRAIL not only contributes to the anti‐HIV‐1 activity of NK cells but also possesses a multifunctional role beyond receptor‐mediated induction of apoptosis, acting as a regulator for the induction of different effector functions.