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Erythroblastosis fetalis
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Avinash Patil, Brian Brocato, Rebecca A. Uhlmann, Giancarlo Mari
Red blood cell (RBC) alloimmunization, or isoimmunization, is the development of maternal antibodies to fetal RBC antigens. Hemolytic disease of the newborn/fetus is a hemolytic anemia that results from the lysis of the fetal RBCs by maternal antibodies. It is often characterized by excessive erythroblasts in the fetal bone marrow and circulation (erythroblastosis fetalis). Other features include generalized edema (hydrops fetalis) and hepatosplenomegaly. Alloimmunization and hemolytic disease of the newborn/fetus most commonly occur when maternal antibodies form against paternally derived Rhesus (D) antigens of the fetus, which is termed Rhesus (Rh) alloimmunization.
The lymphoreticular system and bone marrow
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The marrow is hypercellular, and the erythroblasts are large and show failure of nuclear maturation (megaloblastic change). The combination of increased cellularity and shift to more primitive forms may lead to leukaemia being falsely suspected. It is best to treat megaloblastic anaemia with both vitamin B12 and folate, because supplying one may unmask a deficiency of the other. The anaemia is fully reversible, although in pernicious anaemia maintenance vitamin B12 treatment is required for the rest of the patient's life.
Immunohematology
Published in Gabriel Virella, Medical Immunology, 2019
Gabriel Virella, Armand Glassman
The usual clinical features of this disease are anemia and jaundice present at birth, or more frequently, in the first 24 hours of life. In severe cases, the infant may die in utero. Unless treated appropriately, other severely affected children who survive until the third day develop signs of central nervous system damage, attributed to the high concentrations of unconjugated bilirubin (kernicterus). The peripheral blood shows reticulocytes and circulating erythroblasts (hence the term “erythroblastosis fetalis”).
Decreased expression of HBA1 and HBB genes in acute myeloid leukemia patients and their inhibitory effects on growth of K562 cells
Published in Hematology, 2022
Ping Luo, Xiaoyan Liu, Zehai Tang, Bei Xiong
Erythropoiesis is a process that hematopoietic stem cells (HSCs) differentiate into erythrocytes, including early erythropoiesis and terminal erythroid differentiation [2]. Primitive erythroblasts enucleate to become reticulocytes, which subsequently mature into red blood cells [3,4]. Adult red blood cells, as the terminal differential cells, with no nucleus and rather simple structure, have ceased dividing and have no proliferation capacity [5]. The main feature of red blood cells is a high level of adult hemoglobin, with hemoglobin A (HbA) accounting for 97% of its weight, which indicates that high expression of HbA may be accompanied by the cessation of cell proliferation. Human erythroleukemia K562 cells can proliferate indefinitely, but don’t express HbA. Does this mean that no expression of HbA may be accompanied by unlimited proliferation? HBB and HBA1 are genes that encode the normal adult hemoglobin tetramer (Hb) [6]. Adult hemoglobin (HbA) is the most popular form of hemoglobin including two β-globin molecules and two α-globin molecules [7]. Therefore, we hypothesized that HBB and HBA1 may be associated with differentiation degree and proliferation ability of blood cells.
Luspatercept for β-thalassemia: beyond red blood cell transfusions
Published in Expert Opinion on Biological Therapy, 2021
Ali T. Taher, Maria Domenica Cappellini
β-thalassemia is a hereditary hemoglobinopathy caused by over 400 identified mutations (as of 1 July 2021) of the β-globin gene (HBB) or promoter region that reduce or prevent the expression of the β-globin subunit of hemoglobin (Hb) in erythroid precursors (Figure 1) [1,2]. The resultant defects in Hb production are associated with premature cell death via apoptosis, and a reduction in the rates of late-stage maturation and differentiation of red blood cell (RBC) precursors; ineffective erythropoiesis, anemia, hypoxia, and iron homeostasis dysregulation are the consequences [3]. Ineffective erythropoiesis is a hallmark of β-thalassemia and is characterized by abnormalities in differentiation or maturation of erythroid precursors and apoptosis of erythroblasts, leading to a lower than expected number of mature erythroblasts despite increased proliferation of progenitors [4]. Ineffective erythropoiesis in β-thalassemia may be due to a number of related mechanisms, such as increased apoptosis of erythroid progenitors (possibly at the polychromatic normoblast stage), decreased differentiation of erythroid progenitors (leading to an increased proportion of immature progenitors and a lower proportion of mature cells), and oxidative stress (due to the imbalance in α-globin and β-globin chains and the resultant aggregation and precipitation of free α-globin chains in erythroid progenitors).
Anti-tumor efficacy of a combination therapy with PD-L1 targeted alpha therapy and adoptive cell transfer of PD-1 deficient melanoma-specific human T-lymphocytes
Published in OncoImmunology, 2021
L Marotte, M Capitao, C Deleine, T Beauvais, G Cadiou, J. Perrin, M Chérel, E Scotet, Y Guilloux, F Bruchertseifer, A Morgenstern, A Jarry, J. Gaschet, N Labarriere
Since TAT is delivered through i.v. injection, some hematological toxicity related to ionizing radiation is expected. As already observed in our previous study19, platelet counts were significantly decreased in all groups treated with TAT alone or TAT in combination with melanoma-specific T-cells. More surprisingly, we also observed some toxicity on RBC in all the groups but the one treated with the combination of TAT and WT melanoma-specific T-cells. Although this toxicity does not appear to be directly associated with the treatment, as the same decrease was observed in the control group, it should be considered in future studies. However, this does not appear to be related to erythroblast toxicity since we did not observe any bone marrow toxicity as assessed by Flt3-Ligand levels.