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Hemolytic Disease of the Fetus and Newborn
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Pedro Argoti, Ana M. Angarita, Giancarlo Mari
Hemolysis leads to extramedullary erythropoiesis, reticuloendothelial clearance of RBC, fetal anemia, hydrops and eventually fetal death [15]. The Kell antigen is present in fetal cells early in development and it is also expressed on bone marrow erythroid progenitor cells. Anti-Kell alloimmunization leads to hemolysis of RBC as well as suppression of normal erythropoiesis [16, 17]. The presence of multiple antibodies seems to predict a more rapid decline in fetal hemoglobin [18].
Cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The Kell system is the third most important blood group system after the ABO and Rh systems. The K antigen is present on red cells, leukocytes and platelets. Although the K antigen is immunogenic, it is of relatively low frequency and therefore may only cause isoimmunization in patients who have had multiple blood transfusions.
Inherited Defects in Immune Defenses Leading to Pulmonary Disease
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
A recent series of immunogenetic studies have correlated X-linked CGD with aberrations in a white and red cell tissue surface antigen, Kx. [128,129]. Kx is a membrane antigen present on normal leukocytes, monocytes, and in trace amounts on red cells. It is related to erythrocyte Kell antigens [130-132] and is present in large amounts in persons having the rare Kell null phenotype. In contrast to autosomal Kell genes, Kx is determined by an X-linked gene [133]. It is not unusual for independent gene loci to interact in determining a phenotype of a blood group system.
Identification and management of fetal anemia due to hemolytic disease
Published in Expert Review of Hematology, 2022
Renske M. van ’t Oever, Carolien Zwiers, Derek de Winter, Masja de Haas, Dick Oepkes, Enrico Lopriore, E.J.(Joanne) Verweij
Most of the severe cases of HDFN are caused by alloimmunization against the D antigen, part of the Rh blood group system. Other contributors are antibodies targeting the K antigen (of the Kell blood group system) and c and other Rh antigens. Severe HDFN is seldom caused by other antibodies [1,2]. In the years following the discovery of the cause of HDFN, numerous strategies were introduced to reduce the occurrence of the disease. One of the most beneficial strategies is RhD immunoprohylaxis (RhIg) to prevent formation of alloantibodies against the D antigen. In most high- and medium-income countries, RBC D typing and screening for RBC antibodies is conducted routinely early in pregnancy and in the third trimester. During pregnancy and after the birth of a D-positive child, RhD-negative women are protected against D-immunization by RhIg [3–7].
Autophagy-deficiency in bone marrow mononuclear cells from patients with myasthenia gravis: a possible mechanism of pathogenesis
Published in International Journal of Neuroscience, 2021
Jingqun Tang, Ziming Ye, Yi Liu, Mengxiao Zhou, Liqiang Huang, Qin Mo, Xiaotao Su, Chao Qin
As shown in the previous studies, using flow cytometry and short-term as well as long-term BM cultures, BM progenitor cells and clonogenic assays were assessed, revealing reduction percentage of bone marrow CD34+ cells, disorder proliferative activity of precursors and low clonogenic assay in other AIDs [39,40]. In the current study, we displayed reduction proportion of CD34+ and CD34+CD38+ HSCs in the BM-MNCs fraction. Meanwhile, the clonogenic potential of HPCs was found to be significantly decreased in MG patients as was demonstrated by low CFU-GM in short-term BM culture and reduced CFCs and NACs number in long-term BM culture. These manifestations were more pronounced in GMG. Furthermore, Vaughan JI et al. [41] found that anti-Kell antibodies specifically inhibit the growth of Kell-positive BFU-E and CFU-E, supporting that these antibodies cause fetal alloimmune anemia by suppressing erythropoiesis at the progenitor-cell level. Therefore, we speculated that an abnormal immune milieu may affect the number and functional characteristics of stem cells in MG patients, calling for further studies to elucidate the molecular mechanisms of immune damage.
2-Mercaptoethanol (2-ME)-based IATs or Polybrene method mitigates the interference of daratumumab on blood compatibility tests
Published in Hematology, 2021
Ye Zhou, Leiyu Chen, Tianshu Jiang, Liangfeng Fan, Hang Lei, Yuqing Wang, Hasiyati Heililahong, Jianqing Mi, Danxin Du, Tianhong Miao, Rong Xia, Xuefeng Wang, Dong Xiang, Xiaohong Cai, Xiaofeng Tang
We speculate that the underlying mechanism is similar to the Polybrene method's weak detection ability for Kell blood group antigens. Kell protein, like CD38 molecule, is a type II transmembrane glycoprotein with a single transmembrane, and a carboxyl group outside the cell. Polybrene is a small molecular weight quaternary ammonium that binds to negatively charged molecules on the surface of RBCs [22]. Polybrene method has a weak detection ability for the Kell system's antibody, which is related to the negatively charged carboxyl group at the Kell protein terminal. The positively charged Polybrene molecule binding to the negatively charged Kell protein molecule in a low ionic medium environment interferes with the Kell system's antigen–antibody reaction. Based on the same mechanism, the Polybrene test is insensitive to CD38-related antigen–antibody reaction. Under a low ionic environment, the CD38 molecule carries a negatively charged carboxyl group extracellularly, which easily binds to the Polybrene molecule and interferes with the binding of the CD38 molecule to DARA.