Welcome to the 13th International Congress on Autoimmunity interactive program

Displaying One Session

Date
Tue, 28.02.2023
Session Time
08:00 - 10:00
Room
ALEXANDRA TRIANTI
Session Type
PLENARY SESSIONS

MAI (THE MOSAIC OF AUTOIMMUNITY) AWARDS CEREMONY (LECTURES OF AWARDEES WILL BE PRESENTED IN PS26 - PEARLS IN AUTOIMMUNITY 2022) (ID 986)

Date
Tue, 28.02.2023
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
08:00 - 08:20

APPLICATION OF MACHINE LEARNING IN RHEUMATOLOGY (ID 778)

Date
Tue, 28.02.2023
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
08:20 - 08:45

IS001 - A EUROPEAN REGISTRY IN AUTOIMMUNITY (ID 779)

Date
Tue, 28.02.2023
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
08:45 - 09:10

Abstract

Abstract Body

Registries are an important component for the acquisition of information in medicine. They complement clinical trials that are relevant for approval, above all by collecting real word data, which is important not only for the frequent comorbidities that often lead to exclusion in clinical trials, but also for collecting long-term data on safety and also on the efficacy of old and new substances. In addition to national registries, which provide important information on the health status of entire countries and their medical care, there is above all an unmanageable number of disease- or medication-related registries, especially for rare and complex diseases. The European Reference Network ReConnet has just conducted a comprehensive survey to get an overview of the available data.

These registers, which are mostly country-based, are as heterogeneous as the diseases they aim to record. Most of these registries are start-up financed, their sustainability depends mostly on the initiative of individual scientists or national professional societies, a few are established Europe-wide. In addition, most registries are set up in such a way that they are not fed from data already collected, but require additional input without this being remunerated. In addition, their evaluation is not carried out in a timely manner and relates to an e.g. annual collection of information that can only incompletely depict the care provided.

With the increasing possibilities of information technology, these and other limitations of current registers can be completely eliminated. We will give an example of how routine care, basic science and support for clinical trials can be integrated in a Medical Data Space in such a way that all areas benefit maximally. We are currently developing such a data space under the name CHRONIN as a model for SLE in Europe.

Hide

IS002 - SYSTEMIC SCLEROSIS: FROM BENCH TO BEDSIDE (ID 780)

Date
Tue, 28.02.2023
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
09:10 - 09:35

Abstract

Abstract Body

Systemic scletosis (SSc) is a complex disease characterized by extensive collagen deposition, microvasculopathy and many autoantibodies (autoAbs). Activation of fibroblasts, a prerequisite for collagen production, can be cause vis various stimuli, including TGFβ, IL-6, and PDGF. T cells and B cells are likely inducers of fibroblast activation.

Tcells are oligoclonal in SSc skin lesions and peripheral blood(PB) and are of profibrotic TH2 type, whereas regulatory T cells (Tregs) are impaired. Cytotoxic CD4+Tcells in skin lesions can induce endothelial cell apoptosis. Effector B cells are hyperactivated whereas IL-10-producing regulatory B cells are decreased. B cells can cause fibrosis through interaction with fibroblasts, macrophages and dendritic cells, and through autoabs, many of which have promote fibrosis. In addition, B cells with high affinity for DNA-topoisomerase I(topo I) produce IL-6 and cause fibrosis, whereas low affinity B cells for topo I produce IL-10 and inhibit fibrosis in a mouse SSc model. Ibrutinib, a Bruton’s tyrosine kinase inhibitor, promoted low affinity B cells for topo I in SSc patients and inhibited fibrosis in a mouse SSc model. Induction ot Tregs with low-dose IL-2 administration and JAK/STAT pathway inhibition in SSc mice ameliorated fibrosis.

Many of these bench findings find application as current therapeutic approaches in human SSc and others, such as administration of ibrutinib, as potential therapeutic agents

Hide

IS003 - COVID-19 RELATED VASCULOPATHY AND ITS THERAPY (ID 781)

Date
Tue, 28.02.2023
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
09:35 - 10:00

Abstract

Abstract Body

We describe how SARS-CoV-2 tropism for alveolar type II pneumocytes is associated with a physiological immunothrombosis in the adjacent closely juxtaposed alveolar capillary network and associated arteriolar and venular territory thrombosis.
This a a mechanism to constrain viral replication and generally keeps virus replication limited to the alveolar territory. However, in severe COVID-19 pneumonia, the failure of initial innate immune responses may trigger severe myeloid related inflammation, Robust SARS-CoV-2 antibody responses in the second week of infection may also enhance antibody dependent immune responses in the alveolus to further exacerbate immunothrombosis.

We dubbed this immunopathology as pulmonary intravascular coagulopathy (PIC) that is largely confined to the lungs and is linked to local intra-pulmonary macrophage activation (McGonagle et al Autoimmunity Rev 2020 & Lancet Rheumatology 2020). This immunopathology is distinct from the well-recognised disseminated intravascular coagulation (DIC) and associated macrophage activation syndrome (MAS) that can also be linked to infection but the latter triggers systemic thrombosis and concomitant bleeding whereas PIC is mostly confined to the lungs. We described who this PIC pathology is linked to vasculitiic type pathology in both the lung and systemic circulation.

The fact that immunomodulatory therapy including steroids, anti-cytokine therapy and JAK inhibition show efficacy in severe COVID-19 is likely down to absence of active endothelial infection but rather a dampening of lung tissue immunothrombosis in the post-viral replication phase of COVID-19. An accurate determination of when viral replication stops is incomplete and has implications for optimal therapy for this novel recognised respiratory virus immunopathology
Hide