Recently, in attempts to prolong allograft survival, the possibility of targeting alloreactive memory cells via their IL-7Rα was postulated [38]. Cyclopamine Our current data indicate that this approach would attack only part of the alloreactive memory cells, leaving unaffected the IL-7Rα- cells which, on the contrary, seem

the most harmful alloreactive memory/effector cells. In conclusion, using the multi-parameter MLC–CFSE assay we have shown that allostimulated cells have a highly activated and differentiated phenotype with increased expression of chemokine receptors relevant for migration of T cells into the graft and high expression of effector molecules. In addition, our analysis of patients before transplantation

who are at risk for experiencing an acute cellular rejection episode, versus those who are not, revealed a higher dsp CD8pf and lower percentage of alloreactive IL-7Rα+ CD8+ T cells. However, given the retrospective nature of our present study and the overlap in results of rejectors compared to non-rejectors, it is not possible to predict the outcome of the transplantation with respect to the occurrence of acute rejection on a per-patient basis. Our data point to quantitative and qualitative differences between T cells of a group of patients who will experience acute cellular rejection episodes and those who will not. The predictive value of these parameters needs to be established in a large prospective study. All authors declare no conflicts of interest. This Pritelivir study was supported financially by grants from the Dutch Kidney Foundation (grant C05·2141), the RISET consortium (Sixth Framework Programme of the European Commission) and Novartis Pharma BV. “
“Citation Doncel GF, Joseph T, Thurman AR. Role of semen in HIV-1 transmission: inhibitor or facilitator? Am J Reprod Immunol 2011; 65: 292–301 Sexual transmission of human immunodeficiency virus type 1 (HIV-1) accounts for 60-90%

of new infections, especially in developing selleck compound countries. During male-to-female transmission, the virus is typically deposited in the vagina as cell-free and cell-associated virions carried by semen. But semen is more than just a carrier for HIV-1. Evidence from in vitro and in vivo studies supports both inhibitory and enhancing effects. Intrinsic antiviral activity mediated by cationic antimicrobial peptides, cytotoxicity, and blockage of HIV–dendritic cell interactions are seminal plasma properties that inhibit HIV-1 infection. On the contrary, neutralization of vaginal acidic pH, enhanced virus–target cell attachment by seminal amyloid fibrils, opsonization by complement fragments, and electrostatic interactions are factors that facilitate HIV-1 infection. The end result, i.e., inhibition or enhancement of HIV mucosal infection, in vivo, likely depends on the summation of all these biological effects.