Inhibition of Erythroid Progenitor Cells by Anti-Kell Antibodies in Fetal Alloimmune Anemia

Vaughan, Janet; Manning, Monica; Warwick, Ruth M.; Letsky, Elizabeth A.; Murray, Neil A; Roberts, Irene

doi:10.1056/nejm199803193381204

Cited by 254 publications

(65 citation statements)

References 21 publications

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“…Eight foetuses were followed for 8-12 weeks during the gestational period 23-36 weeks. In agreement with a study by Vaughan et al (1998) our data confirmed that the number of haemopoietic progenitors was not affected in AF when compared to age matched foetuses with no apparent haematological abnormalities (TOP) and therefore haemopoiesis in AF could be considered representative of the normal population (Table 1).…”

Section: Resultssupporting

confidence: 94%

Telomere length dynamics differ in foetal and early post-natal human leukocytes in a longitudinal study

et al. 2008

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Haemopoietic stem cells (HSC) undergo a process of self renewal to constantly maintain blood cell turnover. However, it has become apparent that adult HSC lose their self-renewal ability with age. Telomere shortening in peripheral blood leukocytes has been seen to occur with age and it has been associated with loss of HSC proliferative capacity and cellular ageing. In contrast foetal HSC are known to have greater proliferative capacity than post-natal stem cells. However it is unknown whether they undergo a similar process of telomere shortening. In this study we show a more accentuated rate of telomere loss in leukocytes from pre term infants compared to human foetuses of comparable age followed longitudinally for 8-12 weeks in a longitudinal study. Our results point to a difference in HSC behaviour between foetal and early postnatal life which is independent of age but may be influenced by events at birth itself.

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Section: Resultssupporting

confidence: 94%

Telomere length dynamics differ in foetal and early post-natal human leukocytes in a longitudinal study

et al. 2008

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“…Therefore, the first pregnancy was not affected by HDFN. As anti-K may not only cause hemolysis but also suppression of fetal erythropoiesis [33], affected fetuses may develop severe anemia. Furthermore, Kell antigens are expressed on fetal RBCs as early as 10-11 weeks of gestation [34].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Antenatal Intravenous Immunoglobulin Treatment in Pregnancies at High Risk due to Alloimmunization to Red Blood Cells

Mayer

Hinkson

Hillebrand

et al. 2018

Transfus Med Hemother

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Background: Alloimmunization to red blood cells (RBCs) may result in fetal anemia prior to 20 weeks gestation. The question as to whether early commencement of antenatal treatment with high-dose intravenous immunoglobulins (IVIG) may prevent or at least delay the development of fetal anemia in the presence of alloantibodies to RBCs is highly relevant. Patients and Results: Here we describe a patient with high-titer anti-K and two other severely affected pregnant women with a history of recurrent pregnancy loss due to high-titer anti-D or anti-D plus anti-C. Early commencement of treatment with IVIG (1 g/kg/week) resulted in prevention of intrauterine transfusion (IUT) in the former two cases, and in a significant delay of development of fetal anemia in the remaining case (26 weeks gestation). Conclusion: Based on our findings and of previously published cases, early initiation of treatment of severely alloimmunized women with IVIG (1 g/kg/week) could potentially improve the outcome of fetuses at risk.

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“…Most PRCA patients have a serum factor identified as an IgG antibody that is cytotoxic for erythroblasts. Studying erythroid progenitors in vitro by semisolid media has shown that erythropoietic arrest occurs after the CFU–E stage in 60% of cases [17, 18]or before the BFU–E stage in 30–40% of cases. In cases secondary to chronic lymphocytic leukemia, a T–cell–mediated erythroid growth suppression has been suggested [18, 19].…”

Section: Discussionmentioning

confidence: 99%

Splenic Lymphoma Presenting as Warm Autoimmune Hemolytic Anemia Associated with Pure Red Cell Aplasia

Zeidman¹,

Fradin²,

Barac

et al. 2000

Vox Sanguinis

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Background and Objective: Warm autoimmune hemolytic anemia (AIHA) is a condition in which peripheral red blood cell (RBC) destruction is induced by the presence of an autoantibody. Pure red cell aplasia (PRCA) represents an isolated process of decreased erythropoiesis. The combination of both is quite rare, with a very poor prognosis. We describe a patient with isolated splenic lymphoma whose presentation was a combination of AIHA and PRCA. The patient was resistant to all treatment. Materials and Methods: Erythroid colony assays were performed, in order to compare the effect of the patient's serum on colonies with that of a normal control. Results: The patient's serum significantly suppressed normal erythroid colony growth. A red cell eluate revealed the presence of a warm autoantibody. Conclusions: The patient's serum contained warm autoantibody responsible for peripheral RBC destruction and a humoral factor, perhaps the warm autoantibody, which suppressed bone marrow erythropoiesis. Establishing an early diagnosis, and treatment of the underlying disease might result in a better prognosis.

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Inhibition of Erythroid Progenitor Cells by Anti-Kell Antibodies in Fetal Alloimmune Anemia

Abstract: Anti-Kell antibodies specifically inhibit the growth of Kell-positive erythroid burst-forming units and colony-forming units, a finding that supports the hypothesis that these antibodies cause fetal anemia by suppressing erythropoiesis at the progenitor-cell level.

Cited by 254 publications

References 21 publications

Telomere length dynamics differ in foetal and early post-natal human leukocytes in a longitudinal study

Telomere length dynamics differ in foetal and early post-natal human leukocytes in a longitudinal study

Efficacy of Antenatal Intravenous Immunoglobulin Treatment in Pregnancies at High Risk due to Alloimmunization to Red Blood Cells

Splenic Lymphoma Presenting as Warm Autoimmune Hemolytic Anemia Associated with Pure Red Cell Aplasia

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