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
10:00 - 12:00
Session Icon
Pre Recorded

MENTAL HEALTH IN INFLAMMATORY ARTHRITIS: TREATMENT ACROSS THE BLOOD BRAIN BARRIER

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
10:00 - 10:20
Session Icon
Pre Recorded

NOVEL MECHANISMS AND TREATMENT APPROACHES IN NEUROPSYCHIATRIC LUPUS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
10:20 - 10:40
Session Icon
Pre Recorded

HOLISTIC CHARACTERIZATION OF THE AUTOANTIGEN REPERTOIRE IN CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY VIA AUTOANTIGENOMICS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
10:40 - 10:50
Session Icon
Pre Recorded

Abstract

Background and Aims

To characterize the repertoires of targeted autoantigens in chronic inflammatory demyelinating polyneuropathy (CIDP) for systemic peculiarities, we detected the autoantigens of patients and controls and analyzed them in a holistic way.

Methods

We screened 43 human sera, comprising 22 CIDP patients, 12 patients with other neuropathies (ONP), and 9 apparently healthy controls (HC) via HuProt protein microarrays testing about 16,000 distinct human bait proteins in parallel. Autoantigen repertoires were analyzed via bioinformatical approaches of autoantigenomics: principle component and hierarchical cluster analysis, analysis of the repertoire sizes in disease groups and clinical subgroups, overrepresentation analyses using databases like those of Gene Ontology, Reactome Pathway, and pathway representation.

Results

1) The cohort of CIDP patients was heterogeneous regarding their autoantigen repertoires; 2) the number of the targeted antigens per CIDP patient depended on the clinical situation: intravenous immunoglobulin therapy responders targeted three times more autoantigens than non-responders; 3) a significant part of the autoantibody set specifically targeted proteins involved in anchoring junction components, motile cilium proteins, glycoprotein metabolic processes, and certain signaling pathway proteins; 4) ≥9 out of 23 central signaling proteins of the growth factor receptor pathway are targeted by CIDP-specific antibodies.

Conclusions

The repertoire of targeted autoantigens of CIDP patients differs systematically from those of controls. Considering systemic autoantigenomic approaches in addition to single antibody approaches may help to understand the disease and to discover novel options for improved diagnosis and prognosis.

Hide

SYSTEMIC LUPUS ERYTHEMATOSUS AND CRYPTOCOCCAL INFECTION IN THE CENTRAL NERVOUS SYSTEM

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
10:50 - 11:00
Session Icon
Pre Recorded

Abstract

Background and Aims

Central nervous system (CNS) is an uncommon affected site by cryptococcal infection (CI) in patients with systemic lupus erythematous (SLE), and it can be very difficult to diagnose, especially in patients receiving immunosuppressive therapy, due to the insidious onset and non-specific symptoms. In addition, mortality can be high even with proper treatment.

Methods

The patients reported here were followed at the Rheumatology division of the Hospital of Clinics of the University of Campinas and we retrospectively reviewed their charts and magnetic resonance imaging (MRI) findings.

Results

We report two patients with SLE that presented at the emergency with acute neurologic symptoms. One presented headache, altered visual acuity, photophobia and mental confusion and the other progressive left-sided hemiparesis. In both no SLE disease activity was observed. MRI showed multiple corticosubcortical lesions with contrast enhancement, restricted diffusion, perilesional edema and small hemorrhagic foci. Serum Cryptococcus neoformans capsular antigen test, by the latex agglutination method, was positive in both cases. Patients were treated with amphotericin B with improvement of symptoms

Conclusions

Central nervous system infection by cryptococcus, in patients with systemic lupus erythematosus, should be suspected in cases of unspecific neurological symptoms such as headache and fever. MRI evaluation should be performed to better characterize the sites of lesion, and, depending of them (meningeal enhancement, ventricular dilatation and even nodular enhancement) this differential diagnosis must always be kept in mind especially in patients receiving steroid treatment.

Hide

FEAM: A NOVEL MODULATOR FOR NEUROINFLAMMATION

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
11:00 - 11:10
Session Icon
Pre Recorded

Abstract

Background and Aims

Neural inflammation is regulated by coagulation proteins including activated protein C (aPC) and its endothelial protein c receptor (EPCR) which together activate protease activated receptor 1 (PAR1) inducing anti-inflammatory effects. We have synthesized a novel molecule based on the binding site of FVII/aPC to EPCR (FEAM) and studied its effectiveness in the treatment of neuroinflammation.

Methods

An in- vitro model for neuroinflammation was induced by LPS applied to N9 microglia cells. In-vivo neuroinflammation was induced by LPS systemic injection to ICR mice and behavior was assessed by the stair-case test. Thrombin and aPC activity from cells and brains were measured by enzymatic fluorescence assays. Proliferation was measured by XTT activity assay. Coagulation factors and inflammation markers levels were evaluated by western blot and real-time PCR.

Results

FEAM prevented the LPS induced increased proliferation rate (1 vs 1.5 arbitrary units (aU), p<0.001) and PAR1 expression in N9 (1.7 vs. 1.2, p<0.001). FEAM also prevented the decreased aPC activity induced by LPS (0.46 vs 0.62 aU, p<0.003) and prevented the elevation of coagulation factors (FX and thrombin) and inflammatory markers (TNFα). In the whole animal model FEAM prevented the LPS induced elevated brain thrombin activity and other coagulation and inflammation factors. FEAM treatment induced improvement in general health indices such as weight, learning and memory and mobility.

Conclusions

In conclusion, FEAM modulation of the FVII-aPC-EPCR pathway may shift the thrombin/PAR1 pathway toward aPC-EPCR mediated protective downstream effects.

Hide

TOLEROGENIC EFFECT OF ECTOPIC IL-35IG PRODUCED BY DENDRITIC CELLS IS MEDIATED BY ARGINASE 1

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
11:20 - 11:30
Session Icon
Pre Recorded

Abstract

Background and Aims

IL-35 is a potent immunosuppressive cytokine. Dendritic cells (DCs) are specialized antigen presenting cells directing immune response toward immunity or tolerance depending on many factors, including cytokine milieu and immunoregulatory enzymes. Indoleamine 2,3-dioxigenase 1 (IDO1) and Arginase 1 (Arg1) are metabolic enzymes that, expressed by dendritic cells, contribute to immunoregulation. We aimed to understand the possible role of IDO1 and Arg1 enzymes as potential immunometabolic effectors downstream tolerogenic ectopic IL‐35Ig.

Methods

We transfected a single chain IL-35Ig gene construct in murine splenic DCs (DC35) and assessed any IDO1 and Arg1 activities as resulting from ectopic IL-35Ig expression. In vitro, modulation of Ido1 and Arg1 genes was evaluated by real-time PCR; in vivo, a negative vaccination strategy exploiting peptide-loaded DC35 was set up in order to induce antigen-specific tolerance in mice subsequently challenged with the same peptide in a DTH experiment.

Results

Unlike Ido1, Arg1 expression was induced in vitro in DC35 and conferred an immunosuppressive phenotype on those cells, as revealed by a DTH assay. In particular, the suppressive response obtained in the control group with wild-type DC35 was still observed when IDO1 function was lost in DC35 (Ido/ DC35); on the contrary, it was reverted by Arg1 inhibition in DC35 with the specific catalytic inhibitor nor-NOHA. Moreover, the in vivo onset of a tolerogenic phenotype in DC35 was associated with the detection of CD25+CD39+, rather than Foxp3+, regulatory T cells.

Conclusions

Arg1, but not Ido1, expression in DC35 appears to be an early event responsible for IL-35Ig–mediated immunosuppression observed in DC35-treated mice.

Hide

ELECTROPHYSIOLOGICAL FEATURES OF PERIPHERAL NEUROPATHY IN SYSTEMIC LUPUS ERYTHEMATOSUS AND SJÖGREN´S SYNDROME AND ASSOCIATION WITH SERUM IMMUNE MARKERS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
11:30 - 11:40
Session Icon
Pre Recorded

Abstract

Background and Aims

Peripheral neuropathy in patients with systemic lupus erythematosus (SLE) and Sjögren´s syndrome (SS) represents significant morbidity. Nerve conduction studies (NCS) are the primary diagnostic tool for the diagnosis. This study aims to describe the electrophysiological features of peripheral neuropathy in SLE and SS and evaluate their association with serum immune markers.

Methods

This is a retrospective study based on the medical charts, laboratory, and NCS results of SLE and SS patients treated between 2016-2019 in a high complexity center in Colombia.

Results

We included 55 patients; 51 (92.73%) were female with a median age of 53 (34-62) years. Thirty-one (56.36%) patients had SS, nineteen SLE (34.55%), and five SLE/SS overlap (9.09%). Alterations in NCS were present in 20 (36.36%) patients, characterized mainly as demyelinating (n=14, 70%). SS patients exhibited lower amplitudes and velocities for the ulnar motor nerve (p≤0.050). Whereas, higher latencies with lower velocities were observed for the sensory branch of the ulnar nerve in SLE patients (p≤0.050). Positivity for anti-Smith antibody was significantly associated with a higher left median motor latency (p=0.028), lower left median (p=0.024), and ulnar (p=0.046) motor amplitudes, and lower left median (p=0.049) and right ulnar (p=0.039) sensory amplitudes. Likewise, positivity for anti-cardiolipin IgG antibodies was associated with a higher right median motor latency (p=0.033), higher bilateral ulnar motor latencies (p≤0.05), and lower bilateral ulnar sensory amplitudes (p≤0.050).

figure 1.png

Conclusions

Electrophysiological features significantly differ between SS and SLE patients, particularly for the ulnar nerves. Anti-Sm and Anti-cardiolipin IgG antibodies might be involved in the pathogenesis of autoimmune peripheral neuropathy.

Hide

SJÖGREN SYNDROME: AN UNDIAGNOSED ETIOLOGY FOR FACIAL PAIN: CASE SERIES WITH REVIEW OF NEUROLOGICAL MANIFESTATION OF SJÖGREN SYNDROME

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
10:00 - 12:00
Room
HALL C
Lecture Time
11:40 - 11:50
Session Icon
Pre Recorded

Abstract

Background and Aims

Facial pain is a challenging entity in medicine, and has a wide range of differential diagnoses. Therefore, different disciplines including neurology, otolaryngology, pain medicine, dentistry and neurosurgery may be involved in diagnosis and management of these individuals although rheumatologic etiology of facial pain has been less discussed and recognized.

Methods

In this case series, we catalogued eleven facial pain patients: 7 were diagnosed with trigeminal neuralgia, 3 with atypical facial pain, and 1 with persistent idiopathic facial pain. All patients were evaluated by several specialists including neurologists, dentists, endodontists, otolaryngologists, pain specialists and neurosurgeons. Two patients underwent craniotomy for microvascular decompression with diagnosis of trigeminal neuralgia with no relief.

Results

All patients were female with negative Sjögren’s syndrome antibody but proven by salivary gland biopsy. All but one were positive for ANA. ESR was normal in all patients, but CRP was elevated in three patients. Brain and trigeminal nerve MRI were unremarkable in all patients. Minor salivary gland biopsy confirmed lymphocytic sialadenitis. Lymphocytic sialadenitis is considered histologic hallmark of Sjögren’s syndrome. Lymphocytic sialadenitis is characterized by presence of significant perivascular or periductular lymphocytic infiltrate. All patients but one complained of sicca syndrome. Age of onset for facial pain in all patients except one was before 50.

Conclusions

CNS and cranial nerves involvement, particularly trigeminal nerve involvement that may present with facial pain or headaches, as the main pSS presenting manifestation has been underestimated and under-looked. We recommend painful trigeminal neuropathy secondary to pSS should be considered in differential diagnosis of facial pain particularly in patients who carry PIFP diagnosis.

Hide