A Complex Serological Investigation Involving LW

Giles, Carolyn M.; Lundsgaard, Anne

doi:10.1159/000466484

Cited by 9 publications

(9 citation statements)

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“…The LW antigen also showed weakened expression, although there was no evidence of an anti-LW antibody, as reported in previous cases of LW suppression (Giles & Lundsgaard, 1967: Chown et ul, 1971). In addition, CD44 expression was reduced, although the AnWj antigen, which like CD44 is influenced by the action of the In(Lu) gene, was expressed normally.…”

Section: Discussionsupporting

confidence: 84%

Transient loss of proteins carrying Kell and Lutheran red cell antigens during consecutive relapses of autoimmune thrombocytopenia

et al. 1994

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A patient is described in whom two consecutive relapses of autoimmune thrombocytopenic purpura (AITP) were associated with loss of red cell antigens of the Kell and Lutheran blood group systems respectively. During the second relapse the glycoprotein CD44 and to a lesser extent the LW antigen were also depressed. Both relapses were associated with concomitant production of IgG antibody recognizing high-frequency determinants on the corresponding antigen-carrying protein. Blocking of antigen sites by these antibodies was not the cause of reduced antigen expression, because immunoblotting studies showed absence of Kell protein during the first relapse, and Lutheran protein during the second. On both occasions the red cell changes reverted to normal with disappearance of the antibody as the AITP entered remission. There was no evidence of clonal lymphocyte expansion as demonstrated using immunoglobulin JH and T cell receptor beta chain probes.

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Section: Discussionsupporting

confidence: 84%

Transient loss of proteins carrying Kell and Lutheran red cell antigens during consecutive relapses of autoimmune thrombocytopenia

et al. 1994

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“…Rh null cells lack the LW antigen as well as the CDE antigens and sometimes have abnormalities of Ss and U antigens. The lack of reactivity against Rh null cells made it possible that the autoantibody is a peculiar form of anti-LW and, indeed, the complex serological findings are reminiscent of those described by Giles and Lundsgaard [4] in a patient called Mrs. J., who was group 0 Rh-negative, developed anti-C+D during her first pregnancy, and at the time of delivery was noticed to have a positive direct antiglobulin test which remained for about 6 months. In her serum, as well as anti-CtD, there was another antibody which reacted with Rh-negative but not Rh null cells.…”

Section: Discussionmentioning

confidence: 88%

Development of Rh-Specific Maternal Autoantibodies Following Intensive Plasmapheresis for Rh Immunisation during Pregnancy

Ting¹,

Seeto²

1977

Vox Sanguinis

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Two cases of autoantibody formation following large volume plasmapheresis for rhesus immunisation during pregnancy are described. In each case the autoantibody was directed against the Rh complex but showed a preference for G-positive cells. It is postulated that repeated plasmapheresis in the presence of persistent antigenic stimulation has removed a feedback inhibition of the immune response. The specificity of the alloantibody has broadened resulting in cross-reactivity against self-antigens. The possible implications of these cases in relation to autoimmunity are discussed.

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“…Anti-LW may be produced under four different situations: (1) as an alloantibody in genetically LWnegative individuals (Swanson & Matson, 1964;Chaplin et al, 1985); (2) as an autoantibody in warm autoimmune haemolytic anaemia (Celano & Levine, 1967;Vos et al, 1973); (3) as a drug-induced antibody (Bartlett et al, 1990); and (4) as a transiently produced antibody in a patient with transient depression of LW antigen. The fourth situation has been reported by Giles & Lundsgaard (1967) and Chown et al, (1971). The LW antigens are occasionally weakened transiently, and anti-LW appears simultaneously.…”

mentioning

confidence: 80%

“…The LW antigens are occasionally weakened transiently, and anti-LW appears simultaneously. This phenomenon has been observed during pregnancy (Giles & Lundsgaard, 1967;Chown et al, 1971) and in various immunological diseases, including Hodgkin's disease (Perkins et al, 1977), asthma (Azar et al, 1989) and idiopathic thrombocytopenic purpura (Koyasu et al, 1988). When the patients have recovered or are in remission from their disease, the depressed antigens re-express themselves, and the anti-LW disappears.…”

mentioning

confidence: 95%

Transient depression of LW^a antigen with coincident production of anti‐LW^a repeated in relapses of malignant lymphoma

Komatsu

Kajiwara

1996

Transfusion Medicine

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Three years ago, a 71-year-old female was admitted because of general lymphadenopathy. She had been on medication for hypothroidism, but had no history of pregnancy or blood transfusion. T-cell lymphoma was found. Since then, she has been treated with intermittent chemotherapy. The patient's LWa antigen was depressed during two relapses of the lymphoma and anti-LWa was detected simultaneously on both occasions. When she entered remission after therapy, her LW phenotype converted from LW(a-) to LW(a+), and this was accompanied by the disappearance of anti-LWa. This suggests that LW(a-) was a transient phenotype. In the first relapse, a total of 8 units of D- LW(a+) packed red cells and 20 units of platelets were transfused during 1 month without any haemolytic reaction. In these relapses, nonhaemolytic anaemia, hyper-gamma-globulinaemia and remarkable bone-marrow infiltration with lymphoplasma cells were recognized. She also possessed antithyroglobulin and antimicrosomal antibodies; however, these autoantibodies did not change with the relapses. These results suggests that the recurrent depressions of LWa may be closely related to the underlying disease.

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A Complex Serological Investigation Involving LW

Cited by 9 publications

References 4 publications

Transient loss of proteins carrying Kell and Lutheran red cell antigens during consecutive relapses of autoimmune thrombocytopenia

Transient loss of proteins carrying Kell and Lutheran red cell antigens during consecutive relapses of autoimmune thrombocytopenia

Development of Rh-Specific Maternal Autoantibodies Following Intensive Plasmapheresis for Rh Immunisation during Pregnancy

Transient depression of LW^a antigen with coincident production of anti‐LW^a repeated in relapses of malignant lymphoma

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A Complex Serological Investigation Involving LW

Cited by 9 publications

References 4 publications

Transient loss of proteins carrying Kell and Lutheran red cell antigens during consecutive relapses of autoimmune thrombocytopenia

Transient loss of proteins carrying Kell and Lutheran red cell antigens during consecutive relapses of autoimmune thrombocytopenia

Development of Rh-Specific Maternal Autoantibodies Following Intensive Plasmapheresis for Rh Immunisation during Pregnancy

Transient depression of LWa antigen with coincident production of anti‐LWa repeated in relapses of malignant lymphoma

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Transient depression of LW^a antigen with coincident production of anti‐LW^a repeated in relapses of malignant lymphoma