Anti-BTNL2 polyclonal antibody [Cy5.5]

Although hematopoietic stem cell transplantation (HSCT) has been widely used in the treatment of many diseases, graft-versus-host disease (GVHD) remains a major complication after allogeneic HSCT. Butyrophilin-like 2 (BTNL2) protein has been reported to have the ability to inhibit T cell proliferation in vitro; its ability to inhibit T cell responses in vivo has not been determined. We show here that in vivo administration of recombinant BTNL2-IgG2a Fc (rBTNL2-Ig) fusion protein ameliorates GVHD in mice. This is related to the ability of rBTNL2-Ig to inhibit T cell proliferation, activation and Th1/Th17 cytokine production in vivo. Furthermore, rBTNL2-Ig treatment increases the generation of regulatory T cells. Our results suggest that rBTNL2-Ig has the potential to be used in the prevention and treatment of patients with GVHD.

Osteoarthritis (OA) is known to have an important genetic component and human genetic studies can help unravel the molecular mechanisms responsible for joint damage and nociception involved in OA. Genetic studies in humans have identified molecules involved in signaling cascades that are important for the pathology of the joint components such as the bone morphogenetic protein growth differentiation factor 5 (GDF5). Genomewide association scans (GWAS) in Asians have uncovered a likely role for structural extracellular matrix components (DVWA), and for molecules involved in immune response (HLA class II DQB1 and BTNL2) but these genes are not associated in Caucasian patients. In Caucasians a similar to 300 kilobase region in chromosome 7q22 containing several genes has been found to be reproducibly associated with OA. A recent European GWAS taking advantage of imputation techniques has uncovered a variant in the MCF2L gene as significantly associated with large joint OA. MCF2L is involved in neurotrophin mediated regulation of cell motility in the peripheral nervous system, and thus potentially implicated in nociception in OA. As the number of OA cases with genomewide genotyping increases it is expected that many more reproducible variants implicated in OA will be reported. This article is part of a Special Issue entitled "Osteoarthritis". (C) 2011 Elsevier Inc. All rights reserved.