Isolation of the phagocytosis-inducing IgG-binding antigen on senescent somatic cells

Kay, Marguerite M. B.

doi:10.1038/289491a0

Cited by 156 publications

(141 citation statements)

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“…Although the senescent-cell antigen was first demonstrated on the surface of senescent human erythrocytes (1,2), it has since been demonstrated on the surface of lymphocytes, polymorphonuclear leukocytes, platelets, embryonic kidney cells, and adult liver cells (5). A molecule immunologically related to band 3, the molecule from which senescent-cell antigen is derived, has been observed on all cells examined (28,29).…”

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confidence: 99%

“…The "neo-antigen" is recognized by the antigen binding, Fab, region (3,10,11) of a specific IgG autoantibody in serum that attaches to it and initiates the removal of cells by macrophages (1)(2)(3)(4). A number of studies performed by us (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11) and by others have demonstrated the presence of IgG on senescent, damaged, and stored erythrocytes (12)(13)(14)(15)(16)(17)(18)(19)(20)1). In addition, workers in several laboratories have recently presented evidence that IgG binding is also involved in the removal of erythrocytes in diseases such as thalassemia (21) and sickle cell anemia (22,23).…”

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confidence: 99%

“…We have named the neo-antigen on senescent erythrocytes "senescent-cell antigen" (5). Senescent-cell antigen is a glycosylated 4.5 region polypeptide that appears to be derived from band 3 (5,8,10,(25)(26)(27).…”

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confidence: 99%

“…Senescent-cell antigen is a glycosylated 4.5 region polypeptide that appears to be derived from band 3 (5,8,10,(25)(26)(27). Senescent-cell antigen is located on an extracellular portion of band 3 that includes most ofthe 38-kDa carboxyl-terminal segment and 30% ofthe anion-transport region (27).…”

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confidence: 99%

“…One hypothesis for the removal of senescent erythrocytes is that a "neo-antigen" appears on the surface of senescent cells leading to IgG binding and cellular removal (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). The "neo-antigen" is recognized by the antigen binding, Fab, region (3,10,11) of a specific IgG autoantibody in serum that attaches to it and initiates the removal of cells by macrophages (1)(2)(3)(4).…”

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confidence: 99%

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Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging and IgG binding to erythrocytes.

Kay¹,

Bosman²,

Shapiro³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

102

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Senescent-cell antigen is a "neo-antigen" that appears on the surface of senescent cells and initiates IgG binding and cellular removal. As an approach to evaluating oxidation as a possible mechanism for generation of senescentcell antigen, we studied erythrocytes from vitamin E-deficient rats. Vitamin E is localized primarily in cellular membranes. Its major role is the termination of free-radical chain reactions propagated by the polyunsaturated fatty acids of membrane phospholipids. Results of our studies indicate that erythrocytes of all ages from vitamin E-deficient rats behave like old erythrocytes from normal rats, as determined by their susceptibility to phagocytosis, IgG binding, anion transport ability, and glyceraldehyde-3-phosphate dehydrogenase activity. Increased breakdown products of band 3 were observed with immunoblotting in membranes of erythrocytes from vitamin E-deficient rats. Breakdown products of band 3 are known to increase as cells age in normal individuals. The data suggest that oxidation may be a possible mechanism for erythrocyte aging and generation of senescent-cell antigen in vivo.

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Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging and IgG binding to erythrocytes.

Kay¹,

Bosman²,

Shapiro³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

102

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Maturation of phagosomes containing different erythrophagocytic particles in primary macrophages

Santarino

Vieira

2017

FEBS Open Bio

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Erythrophagocytosis is a physiological process that aims to remove damaged red blood cells from the circulation in order to avoid hemolysis and uncontrolled liberation of iron. Many efforts have been made to understand heme trafficking inside macrophages, but little is known about the maturation of phagosomes containing different types of erythrophagocytic particles with different signals at their surfaces. Therefore, we performed a comparative study on the maturation of phagosomes containing three different models of red blood cells ( RBC ): aged/senescent, complement‐opsonized, and IgG‐opsonized. We also used two types of professional phagocytes: bone marrow‐derived and peritoneal macrophages. By comparing markers from different stages of phagosomal maturation, we found that phagosomes carrying aged RBC reach lysosomes with a delay compared to those containing IgG‐ or complement‐opsonized RBC , in both types of macrophages. These findings contribute to understanding the importance of the different signals at the RBC surface in phagolysosome biogenesis, as well as in the dynamics of RBC removal.

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Erythrophagocytosis in vivo in sickle cell anemia

Solanki

1985

American J Hematol

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Recent observations that the sickle RBC are excessively susceptible to phagocytosis by macrophages in vitro prompted me to look for evidence of in vivo erythrophagocytosis (Ep) in patients with sickle cell anemia ( S S ) . Freshly prepared smears of unmanipulated blood of 27 patients with SS in steady state were examined for Ep by a 500-cell differential white blood cell (WBC) count performed in duplicate. Ten of 27 (37%) S S patients showed Ep (1-6/1,000 WBC or 1-10/100 monocytes). By contrast, no Ep was found in similarly prepared blood smears of 25 normal adult controls and nine splenectomized subjects. The mean hemotocrit value of the Ep(+) S S patients was significantly lower than that of the Ep(-) patients (21.0 f 1.7% vs 24.0 f 2.7% p < 0.01). Considering the rarity of spontaneous Ep in unmanipulated blood from normal subjects and the relative insensitivity of the method used, the finding of Ep in over one third of S S patients indicates a significant membrane injury of the sickle RBC and serves to validate the in vitro observations. The possible role of the %enescence" mechanism in the induction of Ep is discussed.Key words: sickle cell anemia, erythrophagocytosis, RBC senescence INTRODUCTIONOne determinant of hemolysis in sickle cell anemia ( S S ) is the irreversibly sickled cell (ISC). Two studies [ 1,2] have shown an inverse relationship between the red cell lifespan and the proportion of ISCs in the circulating blood. However, this correlation is far from perfect. Furthermore, in doubly heterozygous sickling diseases, eg, sickle cell hemoglobin C disease and sickle cell Pthalassemia, hemolysis occurs in the absence of an appreciable number of ISCs. These observations imply that other determinants of hemolysis must exist. Recent studies of Hebbel and Miller [3] have shown that the SS red blood cells (RBC) are excessively susceptible to erythrophagocytosis by human macrophages in an in vitro system, suggesting a role for the phenomenon in hemolysis. Since spontaneous erythrophagocytosis is extremely rare in unmanipulated blood of normal individuals, I investigated the presence of erythrophagocytosis in the peripheral blood of patients with sickle cell anemia as a means to validate the in vitro findings and to examine the role of blood monocytes in the red cell removal in SS. MATERIALS AND METHODSBlood smears of 27 patients with SS disease (age 19-51 years, mean 36.3) were examined for erythrophagocytosis (Ep) by a 500-cell differential white blood cell 354Solanki count performed in duplicate. Only those patients who were in steady state and had not received red cell transfusions in the preceding 3 months were included. The S S disease was diagnosed by hemoglobin electrophoresis showing a single band in the position of hemoglobin S and the absence of hemoglobin A on cellulose acetate or starch gel at an alkaline pH and agar gel medium at an acid pH, a positive sickling test, clinical evaluation, and family studies when possible. All blood smears were freshly prepared from a drop of blood at the needl...

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Isolation of the phagocytosis-inducing IgG-binding antigen on senescent somatic cells

Cited by 156 publications

References 10 publications

Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging and IgG binding to erythrocytes.

Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging and IgG binding to erythrocytes.

Maturation of phagosomes containing different erythrophagocytic particles in primary macrophages

Erythrophagocytosis in vivo in sickle cell anemia

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