Platelet activation induced by an antiplatelet autoantibody against CD9 antigen and its inhibition by another autoantibody in immune thrombocytopenic purpura

Yanabu, Mutsumasa; Nomura, Shosaku; Fukuroi, Tsutomu; Suzuki, Masahiko; Kawakatsu, Toshihiro; Kakemoto, Hirofumi; Yamaguchi, Kazuyuki; Kokawa, Terutoshi; Yasunaga, Kōjirō

doi:10.1111/j.1365-2141.1993.tb03148.x

Cited by 32 publications

(20 citation statements)

References 30 publications

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“…Our data are supported by the recent findings that autoantibodies detected in a patient with immune thrombocytopenic purpura were similar to monoclonal antibodies to CD9 differentiation cluster antigen [9].…”

supporting

confidence: 94%

Autoantibodies similar to antidifferentiation ones in immune neutropenias

et al. 1998

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Two groups were distinguished among patients with autoimmune neutropenia with manifest antigranulocytic antibodies. One group consisted of patients whose sera reacted with all forms of leukocytes (granulocytes, monocytes, T and B lymphocytes), like CD45 monoclonal antibodies. Sera of patients from the other group reacted only with polymorphonuclear leukocytes and monocytes, similarly as CD13 monoclonal antibodies. Immunologically distinguished types of neutropenia were characterized by a typical chronic or acute clinical course. Key Words: cluster of differentiation antigens; antigranulocytic antibodies; immune neutropeniasImmune neutropenias are little studied serious diseases. Antineutrophilic antibodies detected in patients with neutropenia have not been characterized in sufficient detail [4,5,10]. Recent studies with monoclonal antibodies (Table 1) MATERIALS AND METHODSSera of 15 patients with immune neutropenia aged 1-61 years were examined. Clinically the disease was characterized by acute or chronic neutropenia with or without concomitant bacterial or viral infections or local inflammations. Sera of all patients contained granulocytotoxic antibodies. In the majority of sera these antibodies were detected in titers 1:16-1:128. In three patients the titer of antibodies was no higher than 1:8.Complement-dependent cytotoxic test was the principal method of investigation [8,10]. Serum (1 lal) was pipetted into 60-weU plates under Vaseline oil, an equal volume of suspension with cell concentration of 3000-4000 eells/mm 3 was added, and the mixture was incubated for 1 h with polymorphonuclear leukocytes and monocytes at 4~ and with B and T lymphocytes at 18"C. Then 5 ~tl complement (fresh or lyophilized rabbit serum) was added into each well.The plates were incubated for 1.5 h at ambient temperature, after which the contents of the wells was then discarded and 1 rtl 1% Trypan Blue was added in each well. After 5 rain, the reaction was assessed by counting dead and live ceils. The result was considered positive if at least 50% cells were dead (2 points); no more than 10% cells were dead in control wells with nonimmune AB(IV) serum (0 points).

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confidence: 94%

Autoantibodies similar to antidifferentiation ones in immune neutropenias

et al. 1998

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“…33 We have speculated that some IgG binds to platelets in a specific Fab dependent fashion, causing activation or damage to the platelet. This in turn leads to a change in the platelet membrane and increased non-specific binding of plasma proteins and IgG to the platelet surface.…”

Section: Total Platelet Associated Igg (Paigg)mentioning

confidence: 99%

Laboratory investigation of immune thrombocytopenia.

Warner

Kelton²

1997

J Clin Pathol

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“…The pathological findings also showed marked sequestration of platelets in the lung in which ALI developed. However, some antiplatelet antibodies have been shown to directly activate platelets 7,8…”

Section: Discussionmentioning

confidence: 99%

Antiplatelet antibody may cause delayed transfusion-related acute lung injury

Nomura¹,

Torii²,

Shimizu³

et al. 2011

IJGM

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A 61-year-old woman with lung cancer developed delayed transfusion-related acute lung injury (TRALI) syndrome after transfusion of plasma- and leukoreduced red blood cells (RBCs) for gastrointestinal bleeding due to intestinal metastasis. Acute lung injury (ALI) recurred 31 days after the first ALI episode. Both ALI episodes occurred 48 hours after transfusion. Laboratory examinations revealed the presence of various antileukocyte antibodies including antiplatelet antibody in the recipient’s serum but not in the donors’ serum. The authors speculate that antiplatelet antibodies can have an inhibitory effect in the recipient, which can modulate the bona fide procedure of ALI and lead to a delay in the onset of ALI. This case illustrates the crucial role of a recipient’s platelets in the development of TRALI.

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Platelet activation induced by an antiplatelet autoantibody against CD9 antigen and its inhibition by another autoantibody in immune thrombocytopenic purpura

Cited by 32 publications

References 30 publications

Autoantibodies similar to antidifferentiation ones in immune neutropenias

Autoantibodies similar to antidifferentiation ones in immune neutropenias

Laboratory investigation of immune thrombocytopenia.

Antiplatelet antibody may cause delayed transfusion-related acute lung injury

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