Anti-MS4A1 (C-terminal) polyclonal antibody

A more complete understanding of immune-mediated damage to the coronary arteries in children with Kawasaki disease (KD) is required for improvements in patient treatment and outcomes. We recently reported the transcriptional profile of KD coronary arteritis, and in this study sought to determine protein expression of transcriptionally up-regulated immune genes in KD coronary arteries from the first 2 months after disease onset. We examined the coronary arteries of 12 fatal KD cases and 13 childhood controls for expression of a set of proteins whose genes were highly up-regulated in the KD coronary artery transcriptome: allograft inflammatory factor 1 (AIF1), interleukin 18 (IL-18), CD74, CD1c, CD20 (MS4A1), Toll-like receptor 7 (TLR-7) and Z-DNA binding protein 1 (ZBP1). Immunohistochemistry and immunofluorescence studies were performed to evaluate protein expression and co-localization, respectively. AIF1 was expressed transmurally in KD arteritis and localized to macrophages and myeloid dendritic cells. CD74, which interacts with major histocompatibility complex (MHC) class II on antigen-presenting cells, localized to the intima-media. CD1c, a marker of myeloid dendritic cells, was expressed in a transmural pattern, as were IL-18 and CD20. ZBP1 and TLR-7 were up-regulated compared to controls, but less highly compared to the other proteins. These findings provide evidence of antigen presentation and interferon response in KD arteritis. In combination with prior studies demonstrating T lymphocyte activation, these results demonstrate the complexity of the KD arterial immune response.

Background. Recently, several B cell-related markers have been described to be upregulated during operational tolerance in kidney allograft recipients. Little data exist on these markers during allograft rejection. Methods. In this study, we investigated regulation-associated B-cell phenotypes in peripheral blood mononuclear cells (PBMCs) of kidney transplant recipients with (n = 21) and without (n = 22) acute rejection (AR). We also determined expression levels of the B cell-related genes, MS4A1, TCL1A, and CD79B, in PBMCs and isolated B cells. Patient samples were analyzed before transplantation at discharge and at time of AR before initiation of antirejection therapy or at matching timepoints in patients with stable graft function. Results. On transplantation, the peripheral CD19(+)CD24(hi)CD38(hi) transitional B cell subset strongly declined, regardless of the subsequent occurrence of AR. In contrast, the CD19(+)CD27(+)CD24(hi) subset remained stable after transplantation in both patients groups. MS4A1 gene expression levels in PBMC were comparable between patient groups at all timepoints. In contrast, TCL1A expression levels increased in stable patients, but decreased in patients at the time of AR in both PBMC and isolated B cells. CD79B expression levels in stable patients were unaltered after transplantation in PBMC but showed an increase in the B cell fraction at discharge. At the time of AR, CD79B gene expression was significantly lower compared to stable patients, being most apparent in the B-cell fraction. Conclusion. These results suggest that, in addition to being markers for immunologic unresponsiveness, gene expression levels of TCL1A and CD79B may also identify immune activation in the setting of kidney transplantation.