Presence of CD 16 on Endothelial Cells in Heart Transplant Rejection: an Immunohistochemical Study

Abstract

We studied the distribution of Fc gamma RIII (CD16) in human lymphoid and non-lymphoid tissue by immunohistochemistry and two-colour immunofluorescence. In all tissues except stomach, skin, muscle and heart, infiltrating cells were stained. In tonsil and thymus, the CD16 antibody CLBgran 1 labelled some cells with high endothelial morphology in T-cell areas. Two-colour fluorescence combination of CD16 and antibody to Von Willebrand factor confirmed the endothelial nature of the CLB gran 1-positive cells. Fc gamma RIII expression was also demonstrated by antibody CLBgran11, which detects a product of the Fc gamma RIII-B gene of only the NA1 haplotype. A series of 95 endomyocardial biopsies (EMB) taken after heart transplantation was evaluated for Fc gamma RIII expression. In 18 cases Fc gamma RIII was unambiguously detected on endothelial cells by CD16 antibody CLBgran1. There was a significant correlation between capillary CD16 expression and transplant rejection. We conclude that Fc gamma R expression on endothelium represents endothelial activation found in immunopathological and inflammatory conditions.

Tissue distribution of human IgG Fc receptors CD16, CD32 and CD64: An immunohistochemical study

“…The discrepancy may be ascribed to the difference in study material, and state of activation of the endothelial cells. Elsewhere we have reported on the presence of FcyR class 111 on endothelium in endomyocardial biopsies from patients after heart transplantation that correlated with rejection of the transplant (44). This indicates that the expression of FcyR by endothelium is associated with a state of activation of the cells.…”

Detection of Fcγ receptors on human endothelial cells stimulated with cytokines tumour necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ)

“…Fcg receptors type II and III have been demonstrated in EC in placenta [21], lymphoid tissues, and nerves [22]. The presence of Fcg receptors or FcgR-like bindings has been reported on virusinfected EC [23], neutrophil lysate injured EC [19], as well as EC in transplant hearts undergoing rejection [24]. However, several studies failed to confirm the presence of FcgR on other normal vascular EC [21].…”

“…Therefore, nonstimulated human EC may express low levels of FcgRII and FcgRIII. According to reports, anti-FcgRII and anti-FcgRIII bound to endothelium of nerve vessels [28], placental villi [29], and endocardium of hearts undergoing rejection [24].…”

Expression patterns of CD56+ and CD16+ cells in renal transplant biopsies with acute rejection: Associations with microcirculation injuries and graft survival

“…We also observed a higher number of interstitial CD16+ cells associated with peritubular capillaritis. A previous study found a significant correlation between CD16+ cells in myocardial capillaries and heart transplant rejection suggesting that the presence of FcγRIIIA on capillaries may indicate endothelial activation …”