A Cyclotomic Lattice Based Quasi-Orthogonal STBC for Eight Transmit Antennas

In this letter, we propose a lattice-based full diversity design for rate-one quasi-orthogonal space time block codes (QSTBC) to obtain an improved diversity product for eight transmit antennas where the information bits are mapped into 4-D lattice points instead of the common modulation constellations. Particularly, the diversity product of the proposed code is directly determined by the minimum Euclidean distance of the used lattice and can be improved by using the lattice packing. We show analytically and by using simulation results that the proposed code achieves a larger diversity product than the rate-one QSTBCs reported previously.

A New Restricted Full-Rank Single-Symbol Decodable Design for Four Transmit Antennas

Recently, a single-symbol decodable transmit strategy based on preprocessing at the transmitter has been introduced to decouple the quasi-orthogonal space-time block codes (QOSTBC) with reduced complexity at the receiver [9]. Unfortunately, it does not achieve full diversity, thus suffering from significant performance loss. To tackle this problem, we propose a full diversity scheme with four transmit antennas in this letter. The proposed code is based on a class of restricted full-rank single-symbol decodable design (RFSDD) and has many similar characteristics as the coordinate interleaved orthogonal designs (CIODs), but with a lower peak-to-average ratio (PAR).

Differential Effect of IL-27 on Developing versus Committed Th17 Cells

IIL-27 counters the effect of TGF-beta+IL-6 on naive CD4(+) T cells, resulting in near complete inhibition of de novo Th17 development. In contrast, little is known about the effect of IL-27 on already differentiated Th17 cells. A better understanding of how IL-27 regulates these cells is needed to evaluate the therapeutic potential of IL-27 in Th17 cells-associated diseases. In this study, we show that IL-27 had surprisingly little effect on committed Th17 cells, despite its expression of a functional IL-27R. Contrary to de novo differentiation of Th17 cells, IL-27 did not suppress expression of retinoid-related orphan receptor (ROR)gammat or RORalpha in committed Th17 cells. Consistent with this finding, the frequency of committed Th17 cells and their cytokine secretion remained unaffected by IL-27. Both memory Th17 cells (CD4(+)CD25(-)CD62L(low)) that developed in vivo and encephalitogenic Th17 cells infiltrating the CNS of mice developing experimental autoimmune encephalomyelitis produced similar amounts of IL-17A when reactivated with IL-23 in the absence and presence of exogenous IL-27. Finally, IL-27 failed to suppress encephalitogenicity of Th17 cells in an adoptive transfer of experimental autoimmune encephalomyelitis. Analysis ex vivo of transferred Th17 cells in the spleen and CNS of recipient mice showed that cells retained similar phenotype irrespective of whether cells were treated or not with IL-27. Our data demonstrate that in contrast to inhibition of de novo differentiation of Th17 cells, IL-27 has little or no effect on committed Th17 cells. These findings indicate that therapeutic applications of IL-27 might have a limited efficacy in inflammatory conditions where aggressive Th17 responses have already developed.