Dual mechanism of impairment of interleukin-7 (IL-7) responses in human immunodeficiency virus infection: decreased IL-7 binding and abnormal activation of the JAK/STAT5 pathway.

Interleukin-7 (IL-7) plays a central role in controlling the homeostasis of both naive and long-term-memory CD4(+) T cells. To better understand how human immunodeficiency virus (HIV) perturbs CD4(+) T-cell homeostasis, we performed a detailed analysis of IL-7R expression, IL-7 binding, and IL-7-dependent early and late signaling events in CD4(+) T-cell subsets from viremic and efficiently treated patients. HIV infection differentially affected the expression of IL-7 receptor (IL-7R) chains, with decreases in IL-7Ralpha/CD127 expression in the memory subset and increases in gammac/CD132 expression in all CD4(+) T cells.

Subcutaneous graft of D1 mouse mesenchymal stem cells leads to the formation of a bone-like structure.

Mesenchymal stem cells (MSC) are capable of both self-renewal and multi-lineage differentiation into mesoderm-type cells such as osteoblasts, chondrocytes, adipocytes and myocytes. Together the multipotent nature of MSCs and the facility to expand them in vitro make these cells ideal resources for regenerative medicine, particularly for bone reconstruction, and therefore research efforts focused on defining efficient protocols for directing their differentiation into the requisite lineage. Despite much progress in identifying mechanisms and factors that direct and control in vitro osteogenic differentiation of MSCs, a rapid and simple model to evaluate in vivo tissue formation is still lacking.

Human IL-Rbeta chains form IL-2 binding homodimers.

Two types of functional interleukin-2 receptor (IL-2Ralpha/IL-2Rbeta/gammac and IL-2Rbeta/gammac) have already been characterized in humans. Here we describe a new form consisting of IL-2Rbeta/beta homodimers that assemble spontaneously in the absence of gammac. Co-transfection of COS-7 cells with constructs expressing IL-2Rbeta chains tagged with either HA or MYC sequences results in the formation of IL-2Rbeta:HA/IL-2Rbeta:MYC complexes detectable by coimmunoprecipitation.