Immunologic Mechanisms in Idiopathic and Neonatal Thrombocytopenic Purpura

Harrington, William J.; Sprague, Charles C.; Minnich, Virginia; Moore, Carl V.; Aulvin, Robert C.; Dubach, Reubenia

doi:10.7326/0003-4819-38-3-433

Cited by 335 publications

(7 citation statements)

References 61 publications

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“…102,103 Harrington et al were the first to formally describe neonatal thrombocytopenia in 1953, where two infants were born with significantly decreased platelet counts, delivered from mothers without ITP. 104 Although serological techniques were not available at the time, this was the first identification and report describing what we now know as FNAIT. Shulman et al 105 first identified that maternal alloimmunization and antibodies targeting platelet antigens was the reason for platelet destruction in neonates with the disease.…”

Section: Fetal and Neonatal Alloimmune Thrombocytopeniamentioning

confidence: 93%

Platelets and platelet alloantigens: Lessons from human patients and animal models of fetal and neonatal alloimmune thrombocytopenia

et al. 2015

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Platelets play critical roles in hemostasis and thrombosis. Emerging evidence indicates that they are versatile cells and also involved in many other physiological processes and disease states. Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a life threatening bleeding disorder caused by fetal platelet destruction by maternal alloantibodies developed during pregnancy. Gene polymorphisms cause platelet surface protein incompatibilities between mother and fetus, and ultimately lead to maternal alloimmunization. FNAIT is the most common cause of intracranial hemorrhage in full-term infants and can also lead to intrauterine growth retardation and miscarriage. Proper diagnosis, prevention and treatment of FNAIT is challenging due to insufficient knowledge of the disease and a lack of routine screening as well as its frequent occurrence in first pregnancies. Given the ethical difficulties in performing basic research on human fetuses and neonates, animal models are essential to improve our understanding of the pathogenesis and treatment of FNAIT. The aim of this review is to provide an overview on platelets, hemostasis and thrombocytopenia with a focus on the advancements made in FNAIT by utilizing animal models.

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Section: Fetal and Neonatal Alloimmune Thrombocytopeniamentioning

confidence: 93%

Platelets and platelet alloantigens: Lessons from human patients and animal models of fetal and neonatal alloimmune thrombocytopenia

et al. 2015

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“…In vitro studies have shown that these antibodies bind complement, inhibit megakaryocytopoiesis, and hinder proplatelet formation 117 , 118 . Evidence of their pathogenicity stems from seminal studies in the 1950s and 1960s showing that transfer of plasma from ITP patients induced thrombocytopenia in human recipients without the disease 112 , 119 .…”

Section: Other Autoantibody-mediated Diseases and The Pemphigus Paradmentioning

confidence: 99%

Rituximab therapy in pemphigus and other autoantibody-mediated diseases

Ran

Payne

2017

F1000Res

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Rituximab, a monoclonal antibody targeting the B cell marker CD20, was initially approved in 1997 by the United States Food and Drug Administration (FDA) for the treatment of non-Hodgkin lymphoma. Since that time, rituximab has been FDA-approved for rheumatoid arthritis and vasculitides, such as granulomatosis with polyangiitis and microscopic polyangiitis. Additionally, rituximab has been used off-label in the treatment of numerous other autoimmune diseases, with notable success in pemphigus, an autoantibody-mediated skin blistering disease. The efficacy of rituximab therapy in pemphigus has spurred interest in its potential to treat other autoantibody-mediated diseases. This review summarizes the efficacy of rituximab in pemphigus and examines its off-label use in other select autoantibody-mediated diseases.

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“…The presence of antibodies against platelets has traditionally been considered to play a central role in ITP. For example, autoantibodies against platelet glycoprotein (GP)IIb/IIIa or (GP)Ib/IX could be detected in the majority of patients ( 15 , 16 ). Furthermore, the cellular immune responses of patients with ITP have the characteristic immune tolerance disorder ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

Chronic Pediatric Immune Thrombocytopenia Is Not Associated With Herpes Virus Infection Status

Yan

Luo

et al. 2021

Front. Pediatr.

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Background: Immune thrombocytopenia (ITP) is characterized by non-chronic (transient, <12 months) and chronic (≥12 months) decline in the number of platelets. Herpes virus infections have been shown, in many studies, to be associated with the development of ITP. However, it remains unclear whether the herpes virus infection status is associated with the chronic ITP.Methods: We reviewed 480 primary pediatric patients with ITP in the period from January 2017 to December 2019. The prevalence of herpes virus antibodies including the Cytomegalovirus (CMV), Herpes simplex virus 1 (HSV-1), Herpes simplex virus 2 (HSV-2), and Epstein Barr virus were recorded. The levels of serum complement C3 and C4, T (CD3+, CD4+, CD8+), B (CD19+) lymphocytes, and natural killer (CD16+ 56+) cells were also analyzed. Multivariate analysis was used to evaluate the associations between chronic ITP and herpes virus infection status.Results: Compared with non-chronic, patients with chronic ITP had older age (≥3 years), lower levels of hemoglobin and complement C3, and lower probability of CMV and HSV-2 infections (IgM positive; p < 0.05). Patients with herpes virus infection had lower serum platelet counts (p < 0.001), lower complement C3 levels and lower CD4+/CD8+ cells ratio (p < 0.05). Furthermore, platelet counts were positively correlated with CD4+/CD8+ cells ratios (r = 0.519; p = 0.0078), and negatively correlated with T cells (CD3+: r = −0.458, p = 0.0213; CD8+: r = −0.489, p = 0.0131). Multivariate analysis showed that age (OR, 1.644; 95%CI, 1.007–2.684; p = 0.047) was an adverse risk factor for chronic ITP and CMV IgM positive (OR, 0.241; 95%CI, 0.072–0.814; p = 0.022) had lower risk of chronic ITP development, while other herpes virus infection statuses and clinical features were not.Conclusion: Although herpes virus infections were associated with the onset of ITP, our findings indicated that herpes virus infection status might not be a risk factor for chronic ITP.

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Immunologic Mechanisms in Idiopathic and Neonatal Thrombocytopenic Purpura

Cited by 335 publications

References 61 publications

Platelets and platelet alloantigens: Lessons from human patients and animal models of fetal and neonatal alloimmune thrombocytopenia

Platelets and platelet alloantigens: Lessons from human patients and animal models of fetal and neonatal alloimmune thrombocytopenia

Rituximab therapy in pemphigus and other autoantibody-mediated diseases

Chronic Pediatric Immune Thrombocytopenia Is Not Associated With Herpes Virus Infection Status

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