Monoclonal versus polyclonal anti-D in the treatment of ITP

Lazarus, Alan H.

doi:10.1517/14712598.2013.825243

Cited by 9 publications

(10 citation statements)

References 19 publications

(19 reference statements)

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“…First-line treatments include corticosteroids with or without intravenous IVIg and anti-D [ 166 , 167 ]. Second-line therapies consist of splenectomy and/or immune-suppressive agents such as the B cell-depleting anti-CD20 agent Rituximab, and TPO-receptor agonists such as Romiplostim and Eltrombopag are considered third-line treatments [ 168 ] ( Figure 2 ).…”

Section: Therapies Of Itpmentioning

confidence: 99%

“…This treatment is prepared from the plasma of RhD negative subjects immunized against the D antigen [ 181 ]. However, like IVIg, there are more questions than answers about how this medication exactly works, and several attempts to produce monoclonal versions of anti-D have remained unsuccessful [ 166 ]. In a murine ITP model, it appeared that anti-D-coated erythrocytes competed with antibody-opsonized platelets for FcγIIIA–mediated degradation by splenic macrophages [ 190 ], and they were suggested to have a similar mode of action in patients with ITP [ 189 , 191 ].…”

Section: Therapies Of Itpmentioning

confidence: 99%

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Pathogenesis and Therapeutic Mechanisms in Immune Thrombocytopenia (ITP)

Zufferey

Kapur

Semple

2017

JCM

389

470

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Immune thrombocytopenia (ITP) is a complex autoimmune disease characterized by low platelet counts. The pathogenesis of ITP remains unclear although both antibody-mediated and/or T cell-mediated platelet destruction are key processes. In addition, impairment of T cells, cytokine imbalances, and the contribution of the bone marrow niche have now been recognized to be important. Treatment strategies are aimed at the restoration of platelet counts compatible with adequate hemostasis rather than achieving physiological platelet counts. The first line treatments focus on the inhibition of autoantibody production and platelet degradation, whereas second-line treatments include immunosuppressive drugs, such as Rituximab, and splenectomy. Finally, third-line treatments aim to stimulate platelet production by megakaryocytes. This review discusses the pathophysiology of ITP and how the different treatment modalities affect the pathogenic mechanisms.

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Section: Therapies Of Itpmentioning

confidence: 99%

Section: Therapies Of Itpmentioning

confidence: 99%

Pathogenesis and Therapeutic Mechanisms in Immune Thrombocytopenia (ITP)

Zufferey

Kapur

Semple

2017

JCM

389

470

View full text Add to dashboard Cite

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“…Others have suggested that anti‐HLA antibodies found in anti‐D preparations were responsible for the ITP ameliorative effect . While the results with a single monoclonal anti‐D were disappointing, it could nevertheless be argued that the partial efficacy seen with this monoclonal anti‐D could be evidence for the mechanistic requirement of anti‐D IgG . The recently described fully recombinant anti‐D–like therapeutic, rozrolimupab, composed of 25 recombinant human anti‐D monoclonal antibodies (MoAbs), has been shown to significantly improve ITP in a Phase I/II trial, which strongly suggests in fact that the active component of anti‐D are the anti‐D antibodies themselves.…”

mentioning

confidence: 91%

“…It is widely used to prevent hemolytic disease of the fetus and newborn and to increase platelet (PLT) counts in immune thrombocytopenia (ITP), two clinically distinct situations. The active ingredient(s) of anti‐D are thought to be the polyclonal D‐specific antibodies; however, this has not been demonstrated conclusively. The mechanism of action of anti‐D in ITP amelioration remains unclear and several mechanisms have been proposed .…”

mentioning

confidence: 99%

A monoclonal antibody with anti‐D–like activity in murine immune thrombocytopenia requires Fc domain function for immune thrombocytopenia ameliorative effects

Menard

Seabright

et al. 2015

Transfusion

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“…Rhesus immunoglobulin (anti-D) is a polyclonal immunoglobulin G (IgG) antibody directed against the Rhesus D (RhD) factor present in red blood cells (RBCs). It is thus a type of IVIg collected from the blood of men intentionally immunized with RhD + RBCs (4).…”

Section: Introductionmentioning

confidence: 99%

Treating murine inflammatory diseases with an anti-erythrocyte antibody

et al. 2019

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Treatment of autoimmune and inflammatory diseases typically involves immune suppression. In an opposite strategy, we show that administration of the highly inflammatory erythrocyte-specific antibody Ter119 into mice remodels the monocyte cellular landscape, leading to resolution of inflammatory disease. Ter119 with intact Fc function was unexpectedly therapeutic in the K/BxN serum transfer model of arthritis. Similarly, it rapidly reversed clinical disease progression in collagen antibody-induced arthritis (CAIA) and collagen-induced arthritis and completely corrected CAIA-induced increase in monocyte Fcγ receptor II/III expression. Ter119 dose-dependently induced plasma chemokines CCL2, CCL5, CXCL9, CXCL10, and CCL11 with corresponding alterations in monocyte percentages in the blood and liver within 24 hours. Ter119 attenuated chemokine production from the synovial fluid and prevented the accumulation of inflammatory cells and complement components in the synovium. Ter119 could also accelerate the resolution of hypothermia and pulmonary edema in an acute lung injury model. We conclude that this inflammatory anti-erythrocyte antibody simultaneously triggers a highly efficient anti-inflammatory effect with broad therapeutic potential.

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Monoclonal versus polyclonal anti-D in the treatment of ITP

Cited by 9 publications

References 19 publications

Pathogenesis and Therapeutic Mechanisms in Immune Thrombocytopenia (ITP)

Pathogenesis and Therapeutic Mechanisms in Immune Thrombocytopenia (ITP)

A monoclonal antibody with anti‐D–like activity in murine immune thrombocytopenia requires Fc domain function for immune thrombocytopenia ameliorative effects

Treating murine inflammatory diseases with an anti-erythrocyte antibody

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