Welcome to the Autoimmunity 2021 Congress Calendar

The Meeting will officially run on EEST (GMT + 3 / UTC + 3)

To convert the congress times to your local time Click Here

The viewing of sessions cannot be accessed from this congress calendar.
All sessions are accessible via the Main Lobby at the Virtual Platform.

Icons Legend:  - Live Session   |     - On Demand Session   |     - On Demand with Live Q&A

Displaying One Session

PARALLEL SESSIONS
Session Type
PARALLEL SESSIONS
Session Time
13:30 - 15:30
Session Icon
Pre Recorded

DIFFERENTIAL DIAGNOSIS OF SCLERODERMA AND PSEUDOSCLERODERMA

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
13:30 - 13:50
Session Icon
Pre Recorded

STRATIFICATION AND PREDICTION OF PROGRESSION OF SSC-ILD

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
13:50 - 14:10
Session Icon
Pre Recorded

ANTI-ANGIOTENSIN RECEPTOR ANTIBODIES AS CAUSAL DRIVERS FOR SYSTEMIC SCLEROSIS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
14:10 - 14:30
Session Icon
Pre Recorded

SKIN ANTI-FIBROSIS EFFECT OF CIPLUKAN HERB (PHYSALIS ANGULATA LINN) IN SYSTEMIC SCLEROSIS (A DOUBLE BLIND RANDOMIZED CONTROLLED TRIAL)

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
14:30 - 14:40
Session Icon
Pre Recorded

Abstract

Background and Aims

Systemic sclerosis (SSc) is an autoimmune disease characterized by fibrosis and vascular abnormalities. No drug significantly influences the course of SSc, many patients resistant to standard treatment, it is suspected the addition of Physalis angulata Linn (Ciplukan herb) extract can improve the SSc skin fibrosis. The aim of this study was to evaluate the effect of Ciplukan extract on skin fibrosis based on MRSS, CRP, P1NP in SSc with standard therapy.

Methods

Double-blind randomized clinical trial was performed in SSc with stable disease at RSCM and RSHS (November 2015−March 2017) who met the inclusion criteria, continued the standard therapy. The subjects were randomly divided into two groups: the study group (Ciplukan 3 x 250 mg/day for 12 weeks) and the placebo group. MRSS, CRP, P1NP were performed every 4 weeks until the end of the study.

Results

Fifty-nine subjects, divided into two groups: 29 subjects (in the study group); 30 subjects (in the placebo group), the average age of 41 ± 9 years, the proportion of women: male = 9: 1. There was a significant improvement of skin fibrosis in the study group with a relative decrease in MRSS (35.9%) compared with placebo (6.3%; p <0.001), a relative decrease in P1NP (17.8%) versus placebo (0.7%; p = 0.002), and relative decrease in CRP (16,12%) versus placebo (3,29%; p = 0.181). The adverse effect was mild gastrointestinal symptoms.

Conclusions

Ciplukan extract with dose 3 x 250 mg for 12 weeks as adjuvant therapy on SSc with standard therapy, clinically and statistically improvement of skin fibrosis.

Hide

MIR-29A PLAYS A CRUCIAL ROLE IN THE THERAPEUTIC EFFECT OF ASC-DERIVED EXTRACELLULAR VESICLES IN SYSTEMIC SCLEROSIS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
14:40 - 14:50
Session Icon
Pre Recorded

Abstract

Background and Aims

Systemic sclerosis (SSc) is a life-threatening autoimmune disease with unmet medical need, where mesenchymal stromal/stem cells (MSCs) may represent a promising therapeutic approach. MSCs act primarily through the secretion of soluble factors released within extracellular vesicles (EVs). Here, we investigated the effect of adipose-derived mesenchymal stromal cells (ASCs)-EV in the murine model of hypochlorite (HOCl)-induced SSc and the role of miR-29a, a known anti-fibrotic factor.

Methods

HOCl-SSc was induced by 6-weeks daily intradermal HOCl injections. EV were isolated from ASCs. Groups of 8 mice were treated at day 21 with one intravenous injection of PBS, 2.5x105ASCs, 4x107EV isolated from naive ASCs or ASCs transfected by miR-29a inhibitor or control inhibitor. Skin thickness was measured weekly and skin and lung samples were recovered at euthanasia.

Results

EV significantly reduced skin thickness and the expression levels of fibrotic and inflammatory markers in skin and lung tissues, while increasing the expression of extracellular matrix remodeling markers. Injection of ASCs transfected with miR-29a inhibitor in the murine model of SSc resulted in the loss of their therapeutic effect. Interestingly, the injection of EVs isolated from ASCs transfected with miR-29a inhibitor was not able to reduce the clinical symptoms of SSc.

Conclusions

Systemic injection of ASC-derived EVs exerted a similar therapeutic effect as whole ASCs in the murine model of SSc. This effect was, at least in part, mediated by miR-29a.

Hide

HIGH PREVALENCE OF MALNUTRITION IN SYSTEMIC SCLEROSIS: RESULTS FROM A FRENCH MONOCENTRIC COHORT STUDY

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
14:50 - 15:00
Session Icon
Pre Recorded

Abstract

Background and Aims

Data concerning malnutrition in systemic sclerosis (SSc) are scarce and contradictory, with a poor description of nutritional risks. Herein, we investigated the nutritional status of a cohort of SSc patients.

Methods

Malnutrition was defined as a weight loss of ≥10% in 6 months, or BMI <21kg/m2. We used the« Malnutrition Universal Screening Tool » (MUST) score to stratify nutritional risk.

Results

We included 120 patients suffering from limited (57%), diffuse (21%) and sine sclerodermaSSc (4%). Autoantibodies were anti-centromere (37%), anti-Scl-70 (14%), or double negative (42%). 84% of patients had GI involvement with chronic-intestinal-pseudo-obstruction in about 10% of cases. 57% of patients were considered at risk for malnutrition (MUST ≥1) while malnutrition occurred in 58% of cases during follow-up. Limitation of mouth opening, muscle and myocardial involvements were associated with high nutritional risk (MUST ≥2). Therapeutic nutrition was required in 7,5% of patients.

Conclusions

Herein, malnutrition concerned more than half of the cohort, in contrast to previous studies (10-18%), with no difference in terms of GI involvement. Of interest, we noted an association between muscle, myocardial involvement and malnutrition, that may be related to vitamin or trace elements deficiencies. Although these observations have to be confirmed through prospective studies, early detection of nutritional risk in SSc patients seems of great importance. In that context, the MUST score may be a useful tool.

Hide

MESENCHYMAL STROMAL CELLS FOR SYSTEMIC SCLEROSIS TREATMENT

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
15:00 - 15:10
Session Icon
Pre Recorded

Abstract

Background and Aims

Systemic sclerosis (SSc) is an orphan autoimmune disease characterized by vasculopathy, dysregulation of the immune response, and progressive fibrosis, with patients high morbidity and mortality. Mesenchymal stromal cells (MSC), demonstrating in vitro and in vivo pro-angiogenic, immuno-suppressive, and anti-fibrotic properties, appear a promising stem cell therapy for SSc. This work review how MSC can target SSc key pathological features.

Methods

An extensive literature analysis was based on combined clinical and immunological expertise on systemic sclerosis and on MSC characterization, production and evaluation of their functional properties

Results

MSC, defined by the International Society for Cellular Therapy, show in vitro and in vivo properties which vary according to the donor type (allogeneic or autologous), the tissue sources (bone marrow, adipose tissue or umbilical cord) and the recipient inflammatory micro-environment. Preclinical studies in SSc animal models show reduced skin and lung fibrosis after MSC infusion. First reports of MSC infusion in SSc patients show safety and early efficacy, which results are currently tested in several ongoing clinical trials worldwide.

Conclusions

To increase the success of MSC based clinical trials in SSc, the design and validation of relevant preclinical models and potency assays with good predictive value are required, with adequate clinical study design, based on immune profiling strategies allowing patient screening and follow-up. Ongoing studies will help establish the appropriate choice of MSC source in different clinical settings, optimal MSC characteristics and priming, as well as the method of delivery.

Hide

CXCL4-DNA AND CXCL4-RNA IMMUNE COMPLEXES CONTRIBUTE TO TYPE I INTERFERON SIGNATURE AND MEMORY B-CELL ACTIVATION IN SYSTEMIC SCLEROSIS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
13:30 - 15:30
Room
HALL A
Lecture Time
15:10 - 15:20
Session Icon
Pre Recorded

Abstract

Background and Aims

Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by tissue fibrosis, vasculopathy and autoimmunity. Half of the SSc-patients show a type I interferon signature in blood/tissues, which correlates with poor prognosis. CXCL4 is a chemokine overexpressed in SSc, and by binding to nucleic acids can induce IFN-alpha in plasmacytoid dendritic cells (pDCs). Here we tested the ability of CXCL4-DNA and RNA complexes to drive IFN-alpha production, and activate immune cell other then pDCs.

Methods

We combined X-ray scattering to clarify how CXCL4 binds nuclei acids, and in vitro immune cell experiments, using purified human plasmacytoid dendritic cells (pDCs) and memory B-cells. We analyzed CXCL4-DNA and CXCL4-RNA complexes in circulation and skin of SSc patients by enzyme-immune-sorbent assay (ELISA), and by confocal microscopy of SSc skin biopsies, respectively.

Results

We elucidated an unanticipated mechanism for CXCL4-mediated immune amplification in SSc: CXCL4 organizes not only “self” DNA but also self-RNA into immune complexes that drastically amplify pDC-activation and interferon-alpha production. The same complexes induce the differentiation of antibody secreting plasma cells from human memory B-cells in vitro. Of interest, CXCL4 becomes the target of autoantibodies in SSc, which also correlate with blood IFN-alpha. CXCL4-DNA and -RNAcomplexes were detected in vivo and correlated with IFN-alpha levels in SSc plasma.

Conclusions

Thus, we established a direct link between CXCL4-DNA/CXCL4-RNA complexes and pDCs and memory B-cells activation and differentiation of antibody-secreting plasma cells. These data indicate the potential of strategies that disrupt inflammation in SSc, by inhibiting the self-assembly of CXCL4-DNA and/or CXCL4-RNA complexes.

Hide