Autoimmune Hematologic Complications in Malignant Lymphoproliferative Disorders

Sacks, Peter V.

doi:10.1001/archinte.1974.00320220183031

Cited by 17 publications

(3 citation statements)

References 2 publications

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“…Therefore, it is hardly surprising that several kinds of diseases and disease combinations can occur in individual patients, despite the fact that a GVHR-like pathogenesis may be the common denominator in them all. For instance, maligaant lymphomas including Hodgkin's disease may be associated not only with autoantibodies to erythrocytes (Sacks 1974) and lymphocytes (Grifoni et al 1972), but also with immune-complex glomerulonephritis and/or the nephrotic syndrome (Jackson & Oo 1971, Longmire et al 1973, Mulhgan 1974 in Case Records of the Massachusetts General Hospital 1973). Furthermore, combinations of toxic epidermal necrolysis with malignant lymphoma (Caldwell et al 1967, Lyell 1967 or immime-complex glomerulonephritis (Knimlovsky et al 1974) were reported.…”

Section: Combinations Of Gvhr-like Symptomsmentioning

confidence: 99%

Autoimmunization and Lymphomagenesis in Parent‐F₁ Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?

Gleichmann¹,

Gleichmann

Wilke

1976

Immunological Reviews

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Section: Combinations Of Gvhr-like Symptomsmentioning

confidence: 99%

Autoimmunization and Lymphomagenesis in Parent‐F₁ Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?

Gleichmann¹,

Gleichmann

Wilke

1976

Immunological Reviews

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“…The autoimmune birds described in this paper developed massive lymphoid tumors. The association between generalized autoimmunity and lymphoid neoplasms also exists in individual patients (32) and in NZB mice. NZB mice develop autoantibodies against thymus ceils when they are 1 mo old (33) and subsequently develop anti-RBC, anti-DNA, anti-RNA, and anti-G antibodies (Gross-type murine leukemia virus-related antigen).…”

Section: Discussionmentioning

confidence: 95%

Tolerance and autoimmunity to erythroid differentiation (B-G) major histocompatibility complex alloantigens of the chicken.

Havele¹,

Wegmann²,

Longenecker³

1982

The Journal of Experimental Medicine

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Hematopoietic chimeras were produced at four different stages of ontogeny between two allogeneic strains of chickens. All chimeras produced by parabiosis at day 12 of embryogenesis and the majority (83%) of the ones produced at day 15 by intravenous injection of allogeneic stem cells remained healthy, chimeric, and specifically tolerant at both the humoral and cell-mediated level throughout a long examination period. Chimeras generated at day 17 of embryogenesis demonstrated specific unresponsiveness at the cell-mediated level but produced specific anti-donor alloantibodies directed against erythrocyte-associated major histocompatibility complex (MHC) (B-G) antigens. These chimeras and a minority (17%) of the chimeras generated at day 15 of embryogenesis developed severe antibody-mediated autoimmune hemolytic anemia after the 5th mo of age and succumbed to massive bursal lymphomas and metastases by the 10th mo of age. The immunological and pathological characteristics of these birds appear to reflect an autoimmune state rather than one of tolerance. Erythroid chimeras generated at day 21 of ontogenic development displayed normal levels of GVH reactivity. These birds were eventually able to eliminate the chimeric state and remained healthy until deliberately killed. These results show that there is a critical period in embryogenesis during which the induction of allogeneic erythrocytic chimerism leads to the development, in adult life, of severe autoimmune anemia, B cell lymphomas, and death. B-G MHC antigens are erythroid differentiation antigens of the chicken. Polymorphic determinants on B-G antigens appear to be important cross-reactive determinants (with environmental bacteria), against which a high background immunity exists. Evidence is presented that the immune response to B-G antigens is responsible for the development of autoimmunity and other pathological events that follow and that tolerance to class I MHC antigens (B-F antigens) shared by lymphocytes erythrocytes is maintained at the same time that B-G tolerance is broken.

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“…The inhibitor may be an autoantibody against some humoral factor associated with chemotaxis and phagocytosis. Autoantibodies occur in malignant diseases of the lymphatic system (Seligmann et a1 1965, Sacks 1974. The mechanism of inhibition seems to be different from that in myelomatosis and macroglobulinaemia (Penny & Galton 1966).…”

Section: Discussionmentioning

confidence: 99%

An Inhibitor of Chemotaxis and Phagocytosis in Reticulum Cell Sarcoma

Ruutu

Vuopio

et al. 1975

Scandinavian Journal of Haematology

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In a study of neutrophil functions in haematological disorders using in vitro techniques, a heat‐stable inhibitor of chemotaxis and phagocytosis was demonstrated in the plasma and serum of a 64‐year‐old woman with reticulum cell sarcoma. In partial purification by chromatography, the inhibitory activity could not be separated from IgG. Clinically the patient did not exhibit abnormal susceptibility to infections.

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Autoimmune Hematologic Complications in Malignant Lymphoproliferative Disorders

Cited by 17 publications

References 2 publications

Autoimmunization and Lymphomagenesis in Parent‐F₁ Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?

Autoimmunization and Lymphomagenesis in Parent‐F₁ Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?

Tolerance and autoimmunity to erythroid differentiation (B-G) major histocompatibility complex alloantigens of the chicken.

An Inhibitor of Chemotaxis and Phagocytosis in Reticulum Cell Sarcoma

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Autoimmune Hematologic Complications in Malignant Lymphoproliferative Disorders

Cited by 17 publications

References 2 publications

Autoimmunization and Lymphomagenesis in Parent‐F1 Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?

Autoimmunization and Lymphomagenesis in Parent‐F1 Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?

Tolerance and autoimmunity to erythroid differentiation (B-G) major histocompatibility complex alloantigens of the chicken.

An Inhibitor of Chemotaxis and Phagocytosis in Reticulum Cell Sarcoma

Contact Info

Product

Resources

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Autoimmunization and Lymphomagenesis in Parent‐F₁ Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?

Autoimmunization and Lymphomagenesis in Parent‐F₁ Combinations Differing at the Major Histocompatibility Complex: Model for Spontaneous Disease Caused by Altered Self‐Antigens?