During, and following on from this surgery, he received 6 E-positive and at least 8 M-positive models. to Red Blood Cell Transfusion (R-FACT) study cohort. This cohort includes 505 alloimmunized cases and 1,010 non-alloimmunized matched controls among a primarily Caucasian source populace of 24,063 patients receiving their first and subsequent reddish cell transfusions between January 2005 and December 2013 7-BIA at one of six participating hospitals in the Netherlands, as described earlier.8 A detailed description of our case-control cohort and the methodology used has been published recently.9 In summary, cases were identified as all patients who developed a first transfusion-induced alloantibody during the course of their transfusion history against the antigens: c, C, e, E, K, Cw, Fya, Fyb, Jka, Jkb, Lea, Leb, Lua, Lub, M, N, S, or s. Herein, we considered the last (documented or assumed) antigen mismatched transfusion preceding the first positive screen (i.e., the transfusion) to likely have elicited alloimmunization, and defined this as the implicated transfusion. If this last mismatched transfusion could not be identified due to incomplete donor typing, the last non-tested unit preceding the first positive screen was considered as the implicated transfusion. Based on an incidence density sampling strategy, for each recognized case we randomly sampled two non-alloimmunized control subjects out of the source populace, around the 7-BIA precondition that these controls experienced received at least an comparative quantity of (lifetime) reddish cell transfusions in the same study center as the case. The transfusion in these sampled controls, corresponding to the implicated transfusion of their matched cases, was then marked. Subsequently, we constructed a so-called alloimmunization risk period in both cases and controls, stretching from 30 days before to seven days after this (implicated) transfusion. Finally, we compared the presence of a history of splenectomy at the time of the alloimmunization risk period in cases and controls. The study protocol was approved by the Ethical Review Table in Leiden and by the table of each participating center. At the alloimmunization risk 7-BIA period, splenectomy had been performed in 20 patients, namely one case (0.2%) 19 controls (1.9%) (Table 1). In 12 patients, splenic injury was caused by severe trauma or complicated abdominal medical procedures, while no patient underwent a splenectomy in the context of an autoimmune disease. Sixteen of the splenectomized patients received their implicated (observed numbers of alloimmunized patients within the splenectomized source population. Open in a separate window Only one splenectomized patient developed alloantibodies (patient A). In this patient, anti-E and anti-M were simultaneously detected 23 days after a combined orthotopic liver transplantation and splenectomy. During, and following on from this surgery, he received 6 E-positive and at least 8 M-positive models. Using multivariate logistic regression analysis conditioning around the matched variables plus recognized potential confounders (post-splenectomy CT scanning of the stomach, some functional splenic tissue might have remained after splenectomy which mediated alloimmunization. Third, the specific combination of a donor liver transplant with splenectomy could have caused reddish cell alloimmunization pre-primed lymphocytes derived from the donors liver transplant (i.e., passenger lymphocyte syndrome). A similar mechanism has been reported in a patient developing nonhemolytic anti-M after multiorgan transplant.14 Unfortunately, we could not retrieve the red cell 7-BIA antigenic phenotype of the liver donor to corroborate this hypothesis. Finally, we do not imply an absolute abolishment of reddish cell alloimmunization after splenectomy. Indeed, substantial evidence shows that at least a few asplenic patients are still capable of building a protective immune response following an unconjugated polysaccharide vaccination.15 In Rabbit polyclonal to YY2.The YY1 transcription factor, also known as NF-E1 (human) and Delta or UCRBP (mouse) is ofinterest due to its diverse effects on a wide variety of target genes. YY1 is broadly expressed in awide range of cell types and contains four C-terminal zinc finger motifs of the Cys-Cys-His-Histype and an unusual set of structural motifs at its N-terminal. It binds to downstream elements inseveral vertebrate ribosomal protein genes, where it apparently acts positively to stimulatetranscription and can act either negatively or positively in the context of the immunoglobulin k 3enhancer and immunoglobulin heavy-chain E1 site as well as the P5 promoter of theadeno-associated virus. It thus appears that YY1 is a bifunctional protein, capable of functioning asan activator in some transcriptional control elements and a repressor in others. YY2, a ubiquitouslyexpressed homologue of YY1, can bind to and regulate some promoters known to be controlled byYY1. YY2 contains both transcriptional repression and activation functions, but its exact functionsare still unknown addition, the absence of a functional spleen.