scholarly journals Plasma blood group glycosyltransferase activities after bone marrow transplantation

Blood ◽  
1980 ◽  
Vol 55 (4) ◽  
pp. 699-701 ◽  
Author(s):  
A Yoshida ◽  
GM Schmidt ◽  
KG Blume ◽  
E Beutler

Human blood groups (ABO) are known to be determined by the terminal glycosyl residues attached to common carbohydrate chains of the red cell surface. N-acetylgalactosaminyltransferase (A-enzyme) in blood group A persons and galactosyltransferase (B-enzyme) in blood group B persons are responsible for producing A and B substances on the red cell surface, with both enzymes absent in blood group O persons. The plasma transferase (A - and B-) activity was assayed after the complete replacement of the bone marrow of patients with acute leukemia or aplastic anemia by transplantation bone marrow from donors with ABO blood group differing from the recipient. The patient's blood type completely changed from the recipient's type to the donor's type. However, the A- and B-enzyme activities of the patients changed only slightly after bone marrow transplantation. The results indicate that most of the A- and B-enzymes in the circulatory plasma is not derived from the bone marrow, lymphoid, or macrophage tissue. Other tissues must be the primary source of the enzymes in plasma.

Blood ◽  
1980 ◽  
Vol 55 (4) ◽  
pp. 699-701 ◽  
Author(s):  
A Yoshida ◽  
GM Schmidt ◽  
KG Blume ◽  
E Beutler

Abstract Human blood groups (ABO) are known to be determined by the terminal glycosyl residues attached to common carbohydrate chains of the red cell surface. N-acetylgalactosaminyltransferase (A-enzyme) in blood group A persons and galactosyltransferase (B-enzyme) in blood group B persons are responsible for producing A and B substances on the red cell surface, with both enzymes absent in blood group O persons. The plasma transferase (A - and B-) activity was assayed after the complete replacement of the bone marrow of patients with acute leukemia or aplastic anemia by transplantation bone marrow from donors with ABO blood group differing from the recipient. The patient's blood type completely changed from the recipient's type to the donor's type. However, the A- and B-enzyme activities of the patients changed only slightly after bone marrow transplantation. The results indicate that most of the A- and B-enzymes in the circulatory plasma is not derived from the bone marrow, lymphoid, or macrophage tissue. Other tissues must be the primary source of the enzymes in plasma.


1997 ◽  
Vol 97 (1) ◽  
pp. 141-145 ◽  
Author(s):  
E. C. M. Hendriks ◽  
A. J. M. De Man ◽  
Y. C. M. Van Berkel ◽  
S. Stienstra ◽  
T. De Witte

Blood ◽  
1961 ◽  
Vol 17 (5) ◽  
pp. 610-617 ◽  
Author(s):  
DANIEL G. MILLER

Abstract The sickle cell trait appears to offer a reliable and replicable tag for bone marrow transplantation. Red cell survival curves using sickle cell and nonagglutinable cell counts show good agreement. The recipients exhibited no untoward effects as a result of receiving marrow from a donor with sickle cell trait.


Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 578-582 ◽  
Author(s):  
R Fox ◽  
R McMillan ◽  
W Spruce ◽  
P Tani ◽  
D Mason

Abstract Using monoclonal antibodies to cell surface antigens and fluorescent cell sorter analysis, we studied peripheral blood lymphocyte subsets after bone marrow transplantation (BMT). In 13 patients studied 3 mo or more after BMT, the ratio of T-cell subsets defined by antibodies OKT4 and OKT8 was reversed (OKT4/OK%8 = 0.7 +/- 0.3) in comparison to normal volunteers or bone marrow donors (ratio OKT4/OKT8 = 1.7 +/- 0.4) (p less than 0.001). This reversed ratio persisted for up to 3 yr after BMT. In contrast to a previous report, presence of an abnormal ratio of T-cell subsets did not correlate with clinically significant graft- versus-host disease (GVHD). In agreement with a previous study, (26% +/- 8%; less than 4% in normals (p less than 0.001) and antibody OKT10 reactive cells (39% +/- 20% versus 10% +/- 4%) (p less than 0.01), suggesting in vivo activation. However, their PBL did not react with antibody B3/25 (antitransferrin receptor), a marker found on normal PBL after in vitro activation by mitogens (BMT patients less than 5%; normal PBL T cells plus PHA 45% +/- 11%). These results demonstrate that BMT patients have: (A) an abnormal ratio of T-cell subsets in the presence or absence of clinically significant GVDH disease so that these measurements were not useful in monitoring patients; (B) an increased number of T cells with cell surface phenotype (OKT8+, Ia+, OKT10+, B3/25-) that is distinct from normals but similar to patients with infectious mononucleosis or acquired hypogammaglobulinemia.


Blood ◽  
1971 ◽  
Vol 38 (1) ◽  
pp. 60-65 ◽  
Author(s):  
M. M. AZAR ◽  
R. A. GATTI ◽  
E. J. YUNIS ◽  
J. SWANSON ◽  
R. A. GOOD

Abstract The survival of chromium-labeled group A erythrocytes was measured in a patient who had previously received two bone marrow transplants for reconstitution of lymphopenic hypogammaglobulinemia. The patient was of blood group A before transplantation; the donor of blood group O. The patient’s erythrocytes are now virtually 100% group O. Anti-B titers are present; anti-A antibodies are not demonstrable. The cells producing these isohemagglutinins are of donor origin; the donor has anti-A titers of 1:64 in saline and 1:256 by antihuman globulin test as well as anti-B titers. No evidence of immunological destruction of group A erythrocytes was found in this patient suggesting that the immune system of the donor may have become tolerant of the group A substance of the recipient.


Blood ◽  
1989 ◽  
Vol 74 (2) ◽  
pp. 777-785 ◽  
Author(s):  
JM Kagan ◽  
RE Champlin ◽  
A Saxon

Abstract We investigated the defect in humoral immunity that occurs following bone marrow transplantation (BMT). B cells from BMT recipients were tested for their ability to undergo the sequential steps of activation (RNA synthesis on stimulation with anti-mu or PMA), proliferation (DNA synthesis on stimulation with anti-mu plus B cell growth factor [BCGF], phorbol myristate acetate [PMA], or Staphylococcus aureus Cowan I [SAC] strain bacteria) and differentiation (Ig synthesis stimulated by T cell replacing factor [TRF]). B-cell maturation-associated cell surface markers were simultaneously investigated. “Early” (less than 10 months) posttransplant patients demonstrated defective B-cell activation and also failed to undergo normal proliferation and differentiation. Despite their functional impairment, the early patients' B cells displayed an “activated” phenotype with increased proportions of B cells displaying CD23 (a BCGF receptor) and decreased proportions of Leu 8+ B cells. Furthermore, these patients were uniquely distinguished by the fact that their B cells only weakly (if at all) expressed the CD19 antigen. In contrast, B cells from “late” patients (greater than or equal to 10 months post-BMT) activated and proliferated normally and displayed a normal cell surface phenotype, yet were unable to differentiate to high rate Ig secretion with TRF. Our results suggest a phenotype/function dissociation in early posttransplant period. With time, B cells in BMT patients acquire a normal surface phenotype and can activate and proliferate normally, yet still demonstrate a block in terminal differentiation.


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