Welcome to the 13th International Congress on Autoimmunity interactive program

Displaying One Session

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Room
ALEXANDRA TRIANTI
Session Type
PARALLEL SESSIONS

AUTOINFECTOME: AN HOLISTIC APPROACH TO STUDY PATHOGEN-INDUCED AUTOIMMUNE DISEASE (ID 901)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
17:00 - 17:15

MICROBIAL TRANSGLUTAMINASE IS A NEW POTENTIAL INDUCER OF AUTOIMMUNE DISEASE (ID 900)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
17:15 - 17:30

O088 - IVIG THERAPY- AN UPDATE AND FOCUS ON COVID-19 (ID 707)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
17:30 - 17:40

Abstract

Background and Aims

For a variety of autoimmune diseases, IVIG is an add-on off-label therapy that is beneficial, safe, and may be utilized for long-term therapy.

Methods

IVIG is recommended for patients with concomitant flare and infection. IVIG is beneficial for ICU patients with sepsis or autoimmune disease.

Results

IVIG has many forms (IVIG, sIVIG, scIVIG). sIVIG and scIVIG may be beneficial for COVID-19 infection.

Conclusions

Here, we present an update on IVIG therapy, with the focus on therapy for COVID-19.

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O089 - AN UPDATE ON THE AUTOIMMUNE ASPECTS OF STREPTOCOCCAL INFECTIONS (ID 202)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
17:40 - 17:50

Abstract

Background and Aims

The interplay between the immune system and streptococcal infections in terms of autoimmunity is an old connection documented as early as the 1900s. Acute rheumatic fever (ARF) and acute post-streptococcal glomerulonephritis (APSGN) are good examples of the post-streptococcal autoimmune manifestations.

Methods

ARF most commonly affects children and involves rheumatologic, cardiac, and neurologic manifestations, usually develops 2 to 3 weeks after group A streptococcal pharyngitis. Unsurprisingly, due to the multiorgan involvement of streptococcal infection, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) were also described

Results

In terms of pathophysiology, APSGN was shown to be linked to the interaction of streptococci with the complement system. In turn, immune cells, including B- and T-cells, and macrophages were found to play a critical role in the pathophysiology of ARF by residing in synovium or circulating in the bloodstream attacking antigens in the heart or brain. Furthermore, in regard to vaccines against streptococcal disease, PCV13 which includes aluminum as an adjuvant has been recently described to cause adverse side effects in a form of autoimmune/auto-inflammatory syndrome produced by adjuvants (ASIA)

Conclusions

For instance, PCV13 was reported to result in autoimmune rheumatic disease (AIRD) in addition to serositis caused by autoimmune mechanisms. Interestingly, even though streptococcal coinfection in COVID 19 patients is rare compared with influenza; three case reports concluded that COVID 19 co-infection with S. pneumonia enhances the vulnerability to neuropsychiatric syndromes like PANDAS in the future. Recent aspects of autoimmunity in streptococcal diseases are addressed in our review.

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O090 - INFECTION AND AUTOIMMUNITY: THE EXAMPLE OF PARVOVIRUS (ID 203)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
17:50 - 18:00

Abstract

Background and Aims

For decades, the role of viruses in the initiation and exacerbation of autoimmune disorders have been widely documented. Recently, a growing number of studies have been questioning the relationship between human parvovirus B19 infection and autoimmune disorders. The reason behind a possible association was based on three key findings: 1. the similarities of the clinical manifestations of parvovirus B19 infection with certain autoimmune diseases such as systemic lupus erythematosus (SLE); 2. the production of parvovirus B19 viral protein-induced antibody against self-antigens such as cardiolipin, single-stranded DNA, keratin, and collagen type II; 3. high prevalence of parvovirus B19 DNA as well as positive serological tests of parvovirus B19 in patients with autoimmune diseases. However, the virus-host interactions leading to autoimmune response after parvovirus B19 infection remain uncertain.

Methods

Nevertheless, three mechanisms were proposed as an explanation for evoking an autoimmune response following infection: molecular mimicry, self-antigen presenting to T cells caused by parvovirus B19-induced erythroblast apoptosis, and the phospholipase activity of the unique region of parvovirus B19 VP1 protein. In fact, the importance of revealing the role of parvovirus B19 infection in autoimmune response particularly in the light of new therapeutic perspectives cannot be overemphasized.

Results

Therefore, in our study we review the mechanisms related to autoimmune disorders secondary to parvovirus B19 infection.

Conclusions

Diseases such as SLE, autoimmune-mediated heart diseases like myocarditis and dilated cardiomyopathy, as well as autoimmune hemolytic anemia are all presented and discussed.

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O091 - FERRITIN: FROM HYPERFERRITINEMIA TO COVID-19 (ID 204)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
18:00 - 18:10

Abstract

Background and Aims

It has been known for decades that ferritin is more than an indicator of iron level in the human organism. For instance, ferritin is usually elevated in several infections as well as inflammatory and autoimmune diseases, hence referred as an acute phase reactant. However, there were 4 diseases where ferritin was considered more than just an acute phase reactant, they were collectively classified under the title “hyperferritinemic syndrome”.

Methods

The 4 pathologies that share a common ground of hyperferritinemia are adult-onset Still’s disease (AOSD), catastrophic antiphospholipid syndrome (cAPS), macrophage activation syndrome (MAS), and septic shock. Moreover, the 4 pathologies are potentially life threatening and are usually misdiagnosed. Recent papers suggested ferritin is not only an extremely elevated number in the hyperferritinemic syndrome rather it is involved in the pathogenesis of the diseases.

Results

With the emergence of the pandemic of COVID-19, increased ferritin levels have been documented in patients with severe SARS-CoV-2 infection. The correlation between extremely elevated ferritin levels with the severity of COVID-19 and subsequently the high mortality rate led to the proposal of COVID-19 as the fifth member of the hyperferritinemic syndrome.

Conclusions

In addition to disease severity, prognostic factor, and part of the hyperferritinemic syndrome, the implications of ferritin in COVID-19 went further to include a preventive and therapeutic role in vaccine development and treatment-based approaches. In our discussion we highlight the scientific pathway of ferritin, through inflammation and autoimmunity to COVID-19, forming a solid a base for future investigations aimed to better diagnosis and treat life-threatening diseases.

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O092 - MICROBIAL DIVERSITY IS AFFECTED BY COGNITIVE BEHAVIORAL THERAPY AND MINDFULNESS INTERVENTION AND ACCOMPANIED BY AN INFLAMMATORY RESPONSE IN CROHN'S DISEASE (ID 962)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
18:10 - 18:20

Abstract

Background and Aims

Crohn's disease (CD) is a chronic inflammatory bowel disease associated with psychological stress and intestinal microbial changes. At certain taxonomic levels, the structure of the gut microbiota is significantly altered in CD patients compared to that of healthy individuals. Here, we determined whether a 3-month period of Cognitive Behavioral and Mindfulness-Based Stress Reduction (COBMINDEX), which improved the wellbeing and inflammatory state of CD patients, may also affect their gut microbiome.

Methods

Gut microbiota, circulating inflammatory markers and hormones were studied and compared among 25 CD patients before (T1) and after (T2) COBMINDEX, and 25 matched CD wait-list controls at the corresponding time-points. Microbiota analysis examined relative abundance, alpha and beta diversity measurements, and correlations with inflammatory parameters.

Results

CD patients exhibited a characteristic microbial profile which constitutes mainly of Proteobacteria (%17.71), Firmicutes (%65.56), Actinobacteria (%8.46) and Bacteroidetes (%6.24). Significant changes in beta diversity (Bray-Curtis dissimilarity index) were observed over time in both CD patient groups with an increase among COBMINDEX (p=0.03), and a decrease among wait-list (p=0.00019). Microbial changes in IBD-associated phyla following COBMINDEX, were accompanied by changes in inflammatory markers. Changes in seven untied-to-IBD phyla significantly correlated with inflammatory markers.

Conclusions

Our results show that microbial diversity is connected to the inflammatory profile of CD patients and is significantly affected by COBMINDEX. Linked changes between phyla and inflammatory markers, demonstrated a microbial-inflammatory relationship among CD patients. Lastly, correlations between changes in abundances of untied to CD taxa, with inflammatory markers, hinted new microbial targets in CD.

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O093 - LIVER INJURY UNDER IMMUNE CHECKPOINT INHIBITORS: RESULTS FROM THE FRENCH 'CHILI' STUDY (ID 964)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
18:20 - 18:30

Abstract

Background and Aims

Immune checkpoint inhibitors (ICI) changed the landscape of cancer therapy. Liver toxicity is occurring in up to 25% of patients under ICI. International guidelines recommend pausing immunotherapy and administering corticotherapy, regardless of the hepatitis phenotype. Our study aimed at describing the phenotypes and evolution of ICI-induced hepatitis.

Methods

We conducted an observational study CHILI (CHeckpoint Inhibitors Liver Injury) in patients with ICI-mediated hepatitis through Montpellier «ToxImmun» multidisciplinary meeting between December 2018 and February 2022. Data regarding cancer, hepatitis treatments, and ICI rechallenge were collected. The hepatitis phenotype was defined by the ratio of serum ALT and ALP [R value = (ALT/ULN)/(ALP/ULN)], and categorized as cholestatic (R≤2), hepatocellular (R≥5), or mixed (2<R<5).

Results

From 479 patients discussed, ICI-hepatitis accounted for 12.3% of cases. 59 patients were included (54% men, median age 65). PD-1-inhibitor was the most prescribed ICI class (89.8%), alone (63.5%), or with CTLA-4-inhibitor (30.5%). Hepatitis phenotype was cholestatic in 44%, hepatocellular in 30.5% and mixed in 25.4%. Hepatitis were predominantly grade 3, according to CTCAE (69.5%). No case of severe acute hepatitis was reported. Liver biopsy was performed in 39%. Biliary stenosis occurred in 6 patients (23.1%). An extra-hepatic irAE was reported in 45.9%. Most patients were treated with corticosteroids (76.3%) and ursodeoxycholic acid (UDCA, 35.6%). ICI was resumed in 50.8%, while 63.3% received the same ICI and 96.6 % received a single ICI. The rate of recurrence after ICI rechallenge was 31%.

Conclusions

Future studies should consider adapting the treatment to the hepatitis phenotype, and question the place of UCDA in the case of cholestatic pattern.

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O094 - HIV AND AUTOIMMUNITY- A REVIEW OF LITERATURE (ID 708)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
18:30 - 18:40

Abstract

Background and Aims

Background: Autoimmune diseases in the immune deficient patient with HIV infection or AIDS remain fascinating as both are related to immune dysfunction. The spectrum of reported autoimmune phenomena in HIV infected patients is increasing, especially in AIDS patients that receive highly active anti-retroviral therapy (HAART).

Aims: Rheumatic manifestations due to initial infection of the HIV virus have decreased with the advent of HAART, although the prevalence of autoimmune diseases due to immune restoration inflammatory syndrome (IRIS) has increased.

Methods

Methods: We searched the English language medical literature from the PubMed database published from 2002 to 2021 concerning various autoimmune diseases in HIV and AIDS patients.

Results

Results: Over 300 HIV/AIDS patients with various autoimmune diseases are described

Conclusions

Conclusion: This review will summarize the clinical findings of autoimmune disease in HIV patients through the progression of infection from HIV to AIDS to IRIS.

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O095 - IN SILICO STUDY ON MOLECULAR MIMICRY BASED AUTOIMMUNITY SOURCED BY OMICRON THE VARIANT (ID 983)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
18:40 - 18:50

Abstract

Background and Aims

Molecular mimicry-based autoimmunity has been studied for SARS-CoV-2 and is still under investigation by several research groups. Here we aimed to investigate the potential of mutations at the spike protein of the Omicron variant, as a new means of molecular mimicry.

Methods

Blastp searches of 22 sequences with mutations at the spike protein of Omicron variant (21K and 21L) were performed at NCBI, by limiting the searches to the human proteome. Sequences with similar sequences in the human proteome were manually selected from the results of blastp searches. Then, a second selection was performed to find the subject sequences (human peptides) with less than 5 shared aa with the non-mutant versions of the sequences that they were aligned with. Those sequences were predicted for their binding affinities to the HLA supertype representatives (MHC class I), by using NetCTLpan and NetMHCcons tools (services.healthtech.dtu.dk).

Results

HLA-A*24:02 and HLA-B*15:01 binding affinities for the S371L, S373P, and S375F mutations-region of the spike protein of Omicron 21K, and HLA-A*24:02 affinity for the S371F, S373P, S375F, and T376A mutations-region of that of Omicron 21L, were detected. Human proteins, which are involved, are immunoglobulin kappa chain variable region (sequenceID:ABA71433.1), hCG2003071 (sequenceID:EAW54993.1), and hCG2023603 (sequenceID:EAW76558.1). Sequences of involving Omicron/human peptides are NLAPFFTF/ LLSPFFTF, YNLAPFFTF/ YYLSPFFTY, and NFAPF-FAF/ FAPFLFAF, respectively.

Conclusions

Different from the SARS-CoV-2 infection, if infected with Omicron 21K, individuals with HLA-A*24:02 and HLA-B*15:01 alleles, while if infected with Omicron 21L, individuals with HLA-A*24:02 allele, could be prone to autoimmunity. These results are yet to be verified by experimental studies.

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O096 - MICRONUTRIENT DEFICIENCIES AND METABOLIC STATUS, ASSOCIATIONS WITH INFECTIOUS AND AUTOIMMUNE DISEASES (ID 14)

Date
Sun, 12.06.2022
Session Time
17:00 - 19:00
Session Type
PARALLEL SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
18:50 - 19:00

Abstract

Background and Aims

Autoimmune diseases (ADs) are the most common chronic inflammatory conditions characterized by the loss of self-tolerance, affecting 5-10% of the global population. Although genetic predisposition is a common risk factor for the onset of these diseases, non-hereditary factors seem to be mostly involved in their development. Metabolic complications and micronutrient deficiencies caused by dietary and lifestyle factors encompass common features of ADs, highlighting their shared pathogenetic origin.

Methods

Currently, the clinical management focuses on the treatment of chronic inflammation and reduction of disease outbreaks. However, targeting metabolic perturbations has emerged as promising approach in disease diagnosis and discovery of novel therapeutic targets.

Results

The advantage of this strategy is that it can capture subtle but significant changes that drive disease pathogenesis as metabolic pressure presents before the symptoms occur. The metabolome and the immune system are inherently related networks, considering that maintaining balanced amounts of nutrients is vital to support all the counterparts in the immune system. Metabolic imbalances leading to immune function deregulation involve insulin resistance, alterations in the gut microbiota, defective antioxidant mechanisms, as well as the reduced exposure to physiological germs, a process necessary for the immune system to mature. Biomarker discovery through metabolomics offers the potential to correct the metabolic state and replenish micronutrient deficiencies improving the clinical course in ADs cases.

Conclusions

Overall, metabolomics emerges as a valuable tool in the diagnosis and prevention of ADs onset and, in view of identifying and eliminating the factors that trigger this specific category of diseases.

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