Welcome to the Autoimmunity 2021 Congress Calendar
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NEXT-GENERATION FC RECEPTOR–TARGETING BIOLOGICS FOR AUTOIMMUNE DISEASES [TOPIC: IVIG]
Abstract
Background and Aims
High-dose plasma-derived immunoglobulin (IVIG/SCIG) is a mainstay therapeutic of various autoimmune diseases. Some of the most important effector mechanisms relevant in therapy of autoimmunity are based on the Fc portion of IgG. This includes scavenging of complement and blockade of Fcgamma receptors (FcγR) or neonatal Fc-receptor.
Methods
Recent data indicate that multivalent arrangements of Fc fragments exhibit potent efficacy at substantially lower doses than IVIG. Such approaches include the use of multimerisation domains to link the Fc portions, or by fusing Fc domains to form multivalent molecules. Based on promising preclinical data several molecules of this novel class of biotherapeutics are now being studied in clinical trials.
Results
We investigated the properties of recombinant Fc-hexamers (IgG1-Fc fused to IgM-μ-tailpiece). In vitro, the Fc-hexamers showed high avidity binding to FcγR and C1q. Consequently, they suppressed FcγR -mediated cellular functions and inhibited full activation of the complement system. In vivo, therapeutic treatment of mice with rFc-multimers suppressed inflammatory arthritis and experimental ITP. In a rat model of acute neuromyelitis optica, administration of rFc-multimers reduced brain tissue damage and deposition of C5b-9.
Conclusions
Our data demonstrate potent anti-inflammatory effects of rFc-multimers in models of autoimmunity, supporting their potential as drug candidates for autoantibody mediated diseases
A CENTURY AND STILL GOING STRONG: IVIG IN IMMUNODEFICIENCY AND AUTOIMMUNITY
MULTIPLE INTERSECTIONS BETWEEN SYSTEMIC LUPUS ERYTHEMATOSUS AND IMMUNODEFICIENCY
MANAGEMENT OF SECONDARY ANTIBODY DEFICIENCY WITH INTRAVENOUS IMMUNOGLOBULIN IN PATIENTS WITH PREVIOUS THERAPY WITH RITUXIMAB
Abstract
Background and Aims
Rituximab can be associated with symptomatic secondary antibody deficiency (SAD) in autoimmune diseases (AID). Severe or recurrent infections can develop. There are no established guidelines for evaluating and treating SAD after Rituximab. Intravenous immunoglobulin (IVIG) replacement therapy has been poorly evaluated as treatment for SAD in AID.
Methods
Retrospective analysis of prospectively collected data in a single center. 10 autoimmune disease patients [SLE (2), dermatomyositis (2), vasculitis (2), polymiositis (1), optic neuromyelitis (1), undifferentiated connective tissue disease (n=1), Wegener granulomatosis (1)] that developed severe infections and were found to have SAD after Rituximab. 7 (70%) were women, mean age 62 (39-79). SAD definition: IgG < 600 mg/dL + low anti-pneumococcal antibody titers (anti-PPS<5 mg/dL). Intervention: Non-specific 5% or 10% IVIG at a dose of 400mg/kg/month in addition to conventional antimicrobial therapy with the aims of contributing to control of infection, secondary prevention of re-infection and normalization of IgG (IgG>750 mg/dL). Time of IVIG therapy for analysis: 6 months. Clinical follow up: 6 months after the first dose of IVIG.
Results
A significant increase of IgG levels was demostrated: 865± 133 vs 542±68 mg/dL (p=0.02). A trend towards an increase of anti-PPS was observed: 3.86±1.44 vs 2.98±1.04 (p=0.12). The prevalence of infection was significantly lower during the IVIG period as compared with a similar period of time before IVIG: Infections 1±0.7 vs 3.8±0.8 (p<0.001).
Conclusions
Personalized immunoguided intervention of IVIG in autoimmune disease patients with SAD after Rituximab is associated with lower rates of reinfections. These results require evaluation in a randomized clinical trial.
ANTI-CD45RC MAB IMMUNOTHERAPY CONTROLS THE DEVELOPMENT OF AUTO-IMMUNE SYMPTOMS IN AN APECED RAT MODEL OF AIRE DEFICIENCY
Abstract
Background and Aims
Auto-immune regulator (AIRE) is a key transcription regulator that allows negative selection by promoting the expression of tissue restricted antigens in the thymus. In human, AIRE-deficiency results in the development of autoimmune-polyendocrinopathy-candidiasis-ectodermal-dystrophy (APECED), a lethal autoimmune disease characterized by lesions of multiple peripheral organs and production of many autoantibodies. To date, no cure is available.
Methods
Recently, our team generated the first Aire-/- rat model. In contrast to mouse models, these animals harbor several key features of APECED and are therefore a pertinent model for preclinical studies. We previously showed that targeting CD45RC enables a selective depletion of effector T cells (Teffs) while preserving and boosting regulatory T cells (Tregs). Moreover, anti-CD45RC mAb therapy was protective in transplantation. To address the potential of anti-CD45RC immunotherapy to control APECED autoimmune symptoms, we tested this treatment in our model.
Results
First, we demonstrated that anti-CD45RC mAbs efficiently reduced alopecia and vitiligo presented by Aire-/- animals. Besides, isotype-treated Aire-/- rats showed complete destruction of exocrine pancreas and loss of thymus structure whereas these organs were preserved by anti-CD45RC mAbs therapy. Interestingly, this treatment also decreased the production of autoantibodies and modified Tregs’ transcriptome. Finally, analysis of PBMCs from APECED patients confirmed that the expression of CD45RC was similar to the one observed in Aire-/- rats.
Conclusions
In conclusion, we demonstrated that anti-CD45RC immunotherapy was able to control the development of auto-immune symptoms in Aire-/- rats. Furthermore, CD45RC expression was conserved between our model and APECED patients underlying the clinical potential of CD45RC targeting in this disease.