Procedures to diagnose renal allograft rejection depend upon detection of graft dysfunction and the presence of a mononuclear leukocytic infiltrate; however, the presence of a modest cellular infiltrate is often not conclusive and can be detected in non-rejecting grafts. We have pursued a molecular approach utilizing reverse transcription (

Coordinate CL gene expression in PBLs and the allograft is usually detected. CL gene expression in PBLs is closely associated with a pathologic diagnosis of rejection. CL gene expression in PBLs may serve as a noninvasive method of monitoring for renal allograft rejection.

We previously isolated cDNA clones from a human monocyte library that encoded one member of a family of low‐affinity surface receptors for the Fc domain of IgG (hFcRII‐A). To investigate possible structural and functional heterogeneity among these receptors, we have now isolated two additional cDNAs (hFcRII‐B and hFcRII‐C) from a human placental library, placenta being a good source of FcR‐bearing macrophages and epithelial cells. Three cDNAs encoded related but distinct transmembrane glycoproteins containing two immunoglobulin‐like domains; however, transfected cells produced receptors that were indistinguishable on the basis of ligand binding or reactivity with anti‐hFcRII monoclonal antibodies. The sequences of hFcRII‐A and ‐B were most closely related and were identical except for several amino acid substitutions and one small internal deletion. While the ectodomain of hFcRII‐C was identical to hFcRII‐B, its cytoplasmic tail was unrelated but highly homologous to the corresponding domain of the receptor isoform (mFcRII‐B2) found in murine macrophages. Thus, human FcRII may be derived from at least two alternatively spliced genes. Northern blots revealed little difference in the pattern of expression of hFcRII isoforms among various myeloid and lymphoid cells or cell lines. However, the blots‐‐as well as in situ hybridization and immunohistochemistry‐‐demonstrated that hFcRII‐C (along with a second monocyte marker, the c‐fms encoded CSF‐1 receptor) was expressed in placental syncytiotrophoblasts. Since syncytiotrophoblasts comprise the IgG‐transporting epithelium of the placental villus, these findings suggest that FcR found in the immune system and in certain epithelia may be structurally or functionally related.

A triad of facial palsy, facial edema, and furrowed tongue characterizes Melkersson-Rosenthal syndrome, a rare, noncaseating granulomatous disease of unknown cause. Although most reported cases of Melkersson-Rosenthal syndrome involve swelling of the perioral area, the authors present a case of Melkersson-Rosenthal syndrome involving the periocular area. Because of its rarity, the syndrome is usually ignored and misdiagnosed; however, the syndrome should not only be considered in the classic perioral presentation but also in the rare periocular form, which may be confused with orbital tumors and orbital pseudotumors. Biopsies should be performed routinely in all patients who present with eyelid edema of unknown etiology. The physician and surgeon who see patients with head and neck pathology should be familiar with Melkersson-Rosenthal syndrome, and with the possibility of its presentation in the orbit and periocular region.

Bacteroidesfragilis, an anaerobic bacterium that accounts for only a small fraction of the colonic microflora, is the most frequently isolated anaerobic species in many infectious processes (1), including intraabdominal sepsis (2). Strains of B. fragilis have a polysaccharide antigen on their surface that is not present on other Bacteroides species (3, 4). B. fragilis is unique among anaerobes in its ability to induce abscesses by itself, and in a rat model of intraabdominal sepsis, this ability has been shown to be dependent upon the presence of the polysaccharide capsule (5, 6). It has been shown that rats immunized with this capsular polysaccharide (CP) 1 are protected from intraabdominal abscess formation and bacteremia caused by this organism (7). In the rat, this protection can be passively transferred by nylon wool nonadherent spleen cells (8).To better define the immune response to B. fragilis, we have developed a new experimental model for intraabdominal sepsis using the mouse. This model has several features that make it preferable to other previously described model systems (5, 9). The rat model of intraabdominal sepsis (5) has the disadvantage of requiring surgical implantation of the inoculum, and both a gelatin capsule and BaSO4 are required in order to obtain uniform abscess development. The murine model described by Joiner et al. (9) involved subcutaneous implantation of the inoculum, resulting in subcutaneous abscesses at the site of inoculation. The model described below more closely parallels disease in humans because no vehicle is required, and the result is intraperitoneal abscess formation. The use of sterile cecal contents provides a medium similar to that encountered in naturally occurring intraabdominal sepsis.In the studies detailed below, we have shown that mice immunized with CP are immune to the development of abscesses, and that this immunity is a function of T cells. The immune response is mediated by an antigen-specific, but non-H-2-restricted Ly-l-2 + cell. The application of this model to the study of immune responses to Tindependent polysaccharides is discussed.

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IL-15, a novel growth factor made by a variety of cells, stimulates T cell proliferation in a fashion similar to IL-2. IL-2 transcripts are not routinely found in rejecting human renal allografts at the time of clinically evident rejection. However, T cell proliferation continues as the rejection progresses. We postulated that IL-15 may be actively transcribed during clinical rejection and account, at least in part, for the ongoing T cell expansion. RNA was extracted from renal biopsies and reverse transcribed to cDNA which was used as template for competitive PCR. IL-2 mRNA was detected in just 3 of the 45 biopsy samples. IL-15 transcripts were detected in all renal biopsy specimens and was significantly increased in specimens obtained from rejecting as compared with nonrejecting renal allografts. IL-15 transcription correlates with rejection and may play an important role in T cell mediated rejection.

BackgroundIn December 2014, China announced that only voluntarily donated organs from citizens would be used for transplantation after January 1, 2015. Many medical professionals worldwide believe that China has stopped using organs from death-row prisoners.DiscussionIn the present article, we briefly review the historical development of organ procurement from death-row prisoners in China and comprehensively analyze the social-political background and the legal basis of the announcement. The announcement was not accompanied by any change in organ sourcing legislations or regulations. As a fact, the use of prisoner organs remains legal in China. Even after January 2015, key Chinese transplant officials have repeatedly stated that death-row prisoners have the same right as regular citizens to “voluntarily donate” organs. This perpetuates an unethical organ procurement system in ongoing violation of international standards.ConclusionsOrgan sourcing from death-row prisoners has not stopped in China. The 2014 announcement refers to the intention to stop the use of organs illegally harvested without the consent of the prisoners. Prisoner organs procured with “consent” are now simply labelled as “voluntarily donations from citizens”. The semantic switch may whitewash sourcing from both death-row prisoners and prisoners of conscience. China can gain credibility only by enacting new legislation prohibiting use of prisoner organs and by making its organ sourcing system open to international inspections. Until international ethical standards are transparently met, sanctions should remain.Electronic supplementary materialThe online version of this article (doi:10.1186/s12910-015-0074-0) contains supplementary material, which is available to authorized users.