Welcome to the Autoimmunity 2021 Congress Calendar

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Displaying One Session

PARALLEL SESSIONS
Session Type
PARALLEL SESSIONS
Session Time
15:30 - 17:30
Session Icon
Pre Recorded

PRE-CLINICAL RESEARCH IN VIVO: PROS AND CRONS OF THE C3H/HEJ VERSUS HUMANIZED MOUSE MODE

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
15:30 - 15:50
Session Icon
Pre Recorded

MODULATION OF ANTI-MYELOPEROXIDASE ANTIBODIES MEDIATED NEUTROPHIL ACTIVATION IN VASCULITIS.

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
15:50 - 16:10
Presenter
Session Icon
Pre Recorded

EXPERIMENTAL MODELS IN PEMPHIGUS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
16:10 - 16:30
Session Icon
Pre Recorded

A NEW MURINE MODEL OF VITILIGO-LIKE DEPIGMENTATION INDUCED BY MIA (MELANOMA INHIBITORY ACTIVITY) PROTEIN: A NEW INSIGHT IN THE PATHOGENETIC HYPOTHESES OF VITILIGO.

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
16:30 - 16:40
Session Icon
Pre Recorded

Abstract

Background and Aims

Vitiligo is a disorder of the skin affecting 1% of world population. Even if the role of immune system seems to be well-established, the pathogenesis of the disease remains unclear. We Investigated the role of MIA (melanoma inhibitory protein) in a new mouse model of development of vitiligo-like patchtes after having previously observed that MIA is present in the skin of patients and interacts with proteins which keep melanocytes firmly attached to the basal membrane.

Methods

C57/Bl6 mice (n=10 per conditions) were treated in the tail every 15 days for 3 months with saline (control) or MIA 1% solution to induce pigment loss. Depigmentation spots were scored by blinded observators. Histological examination was performed to evaluate the differences between normal and pigmented skin, melanocytes and inflammatory markers.

Results

The control group did not show any sign of depigmentation. The treated group showed, instead, clear zones of complete depigmentation with the appearance of white patches with whitening of the hair and a clear-cut edge. Histology showed the absence of melanocytes, without presence of inflammatory cells. According to our data, melanocytes are not only directly destroyed by the immune system but detach from the basal membrane toward the stratum corneum and exfoliate together with the surrounding keratinocytes, creating the depigmented macules.

Conclusions

This study demonstrates that MIA protein is able itself to create a vitiligo-like patch by detaching the melanocytes from the basal membrane providing experimental evidence that not only an autoimmune pathway seems to be related to the vitiligo-like depigmentation.

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PROGRESSION OF AUTOIMMUNITY AND FAILURE OF REPRODUCTION – LESSONS FROM THE ANIMAL MODELS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
16:40 - 16:50
Session Icon
Pre Recorded

Abstract

Background and Aims

Systemic Lupus Erythematosus (SLE) is a polygenic autoimmune disorder involving multiple organs that can influence female fertility. MRL/lpr and Pristane-induced mouse models of SLE are very suitable to study female fertility compared to the healthy animals with the same background.

Methods

Lupus-like symptoms were induced through intraperitoneal injection of hydrocarbon oil pristane in non-autoimmune Balb/c mice. Flow cytometry was used for detection of activation markers and apoptosis assay. The levels of cytokines, autoantibodies and the number of autoantibody-producing plasmocytes were quantified by ELISA, ELISpot and protein array.

After hormonal ovarian stimulation, ovulated oocytes were derived from oviducts. Chromatin, tubulin and actin structures were detected by Hoechst 33258, FITC-labeled alpha-tubulin antibody and rhodamine-labeled phalloidin, respectively.

Results

A single i.p. injection of pristane leads to the development of the typical SLE symptoms such as production of different autoantibodies accompanied by massive glomerular depositions of IgG-containing immune complexes in the kidneys, and proteinuria.

The total number of obtained metaphase oocytes from lupus mice was significantly lower compared to healthy controls. The maturation rate, i.e. the proportion of eggs reaching metaphase II, was also lower for Lupus mice compared to control animals.

For each oocyte, four characteristics were described – spindle morphology, actin cap, chromosomal condensation and alignment. Many specific abnormalities in the lupus group were found.

Conclusions

Pristane-induced and MRL/lpr mouse models of lupus exhibited numerous impairments of the reproductive system which may result due to disease activity, autoantibodies or damage in molecular mechanisms through the process of reproduction.

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STUDY OF THE CONCENTRATION OF SMALL FRACTION IMMUNE COMPLEXES IN THE TISSUES OF EXPERIMENTAL WHITE MICE UNDER CONDITIONS OF IMMOBILIZATION STRESS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
16:50 - 17:00
Session Icon
Pre Recorded

Abstract

Background and Aims

Immobilization stress plays a crucial role in autoimmune reactions. Smll fractions of circular immune complexes (CIC) reflect these physiological changes.

Methods

The study of humoral immune reactions was carried out with the participation of 160 white mice of both sexes, weighing 18-23 g. Humoral immunity indicators were determined by conventional methods: quantitative determination of murine cytokines - IL-1b and IL-10 in blood serum was carried out by enzyme-linked immunosorbent assay using test kits manufactured by Bender MedSystems CJSC BioChemMak (Moscow); components of the complement system were studied by the hemolytic method of E. Kabat and M. Mayer.

Results

The restriction of the motor regime of animals in combination with injection stress led to an imbalance of humoral immune responses. The degree of change in the studied parameters depended on the duration of the stressful effect. After 1 day, IP plasma concentrations of pro-inflammatory and anti-inflammatory cytokines, components of the complement system, IC concentration in the tissues of internal organs did not change relative to the group of intact animals.
By the 5th day of immobilization, pronounced changes in indicators of humoral immunity persisted. There was a decrease in the complementary activity of blood serum mainly due to the C1, C4 and C5 components of complement. A significant increase in the formation ofCIC) was observed: the number of large CICs increased by an order of magnitude, medium and small by 3 and 2 times, respectively.

Conclusions

CIC from different organs were found in different concentrations, which show various scenarios of autoimmune responces.

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IGG FROM PATIENTS WITH CHRONIC FATIGUE SYNDROME AND ANTI AUTONOMIC ANTIBODIES BIND SPECIFIC STRUCTURES IN THE SKIN

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
17:00 - 17:10
Presenter
Session Icon
Pre Recorded

Abstract

Background and Aims

A group of diseases including fibromyalgia and chronic fatigue syndrome (CFS) are commonly associated with small fiber neuropathy and with autonomic dysfunction. We therefore tested whether IgG from CFS patients binds to structures in the skin.

Methods

IgG was purified from patients with CFS who had high levels of antibodies to the autonomic adrenergic and muscarinic receptors and whose symptoms improved following plasma immunoadsorption therapy. Mouse skin samples were fluorescently stained with four IgG samples and with pooled control human IgG.

Results

Specific staining of blood vessels in the sub-dermis and dermis were seen in all 4 samples and not in the controls. Some staining of wider epidermal areas was seen in some of the CFS samples while fainter but similar staining was seen in the controls.

Conclusions

CFS IgG binds to blood vessels in the dermis-epidermis areas, possibly through binding to adrenergic or muscarinic receptors. These antibodies may play a role in the pain and skin changes reported in these patients.

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LOW-DOSE INTERLEUKIN-2: BIOLOGY AND THERAPEUTIC PROSPECTS IN RHEUMATOID ARTHRITIS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
17:10 - 17:20
Presenter
Session Icon
Pre Recorded

Abstract

Background and Aims

Rheumatoid arthritis (RA) is a chronic aggressive arthritis. It is necessary to find effective treatment strategies for RA from the pathogenesis of it.

Methods

Summarize the biology of IL-2 and the role of IL-2-mediated immune tolerance in RA to clarify its therapeutic prospect

Results

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One the key pathogenesis of RA is the breakdown of immune tolerance caused by the imbalance of CD4+T lymphocyte subsets. It has been confirmed that T helper (Th) 17 cells can promote inflamma­tion by producing many pro-inflammatory cytokines, while regulatory T (Treg) cells can maintain immune tolerance .T follicular helper (Tfh) cells can produce abnormal antibodies to recognize the antigens in joints to form immune complexes deposited on synovial tissue leading to the persistent synovitis and the destruction of joints, conversely, T follicular regulatory (Tfr) cells can exert an opposite effect in regulating the humoral immunity. It has showed that the imbalance of Th17/Treg cells and Tfh/Tfr cells are related to the progression of RA, reversal of which appears to be a potential therapeutic target for RA. IL-2 has shifted from a pro-inflammatory cytokine to an anti-inflammatory cytokine maintaining immune tolerance, revealing the pleiotropic function of it. Low-dose IL-2 therapy drives the imbalance between autoimmunity and immune tolerance towards immune tolerance, which has been tried to treat autoimmune diseases including RA but it is still a new field with some challenges.

Conclusions

It needs further animal and clinical trials to realize targeted treatment for RA by low-dose IL-2 more effective and safer as the new revolution in immunoregulation.

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A HISTORICAL PERSPECTIVE AND LESSONS LEARNED FROM THE NZB/W F1 MOUSE MODEL FOR SJÖGREN’S SYNDROME AND LUPUS

Session Type
PARALLEL SESSIONS
Date
30.05.2021, Sunday
Session Time
15:30 - 17:30
Room
HALL D
Lecture Time
17:20 - 17:30
Session Icon
Pre Recorded

Abstract

Background and Aims

Sjögren's syndrome (SS) is a chronic autoimmune disorder affecting multiple organ systems. Several animal model systems have been developed to understand the pathogenic mechanisms in the disease process. The lupus-prone New Zealand Black (NZB) x New Zealand White (NZW) F1 (NZB/W F1) mouse represents the first spontaneous mouse model of SS. In this review, we evaluated the utility of the NZB/W F1 mouse to study SS.

Methods

Pubmed searches were conducted using different combinations of search terms: Autoantibody, Histopathology, Lacrimal Gland, NZB, NZW, Saliva, Salivary Gland, Sjögren's Syndrome, Tears, and Therapeutic.

Results

We identified 195 articles for further reading and short-listed 99 articles for inclusion in this review. The NZB/W F1 mouse fulfills 3 objective criteria in the current classification scheme for SS. Histopathology of sub-mandibular glands shows severe sialadenitis with a focus score of more than 1.0; the mice are positive for ANA, RF, and cryoglobulins; and the mice show a progressive decline in salivary and lacrimal gland function. The activation of innate immunity accelerates glandular dysfunction and sialadenitis. However, there is a dissociation between the severity of sialadenitis and the loss of saliva production. The most promising strategy to treat SS-like disease in NZB/W F1 mice seems to be calorie restriction and the recent use of anti-CD40.

Conclusions

The NZB/W F1 mouse represents polyautoimmunity in SS. It is plausible that such patients will require distinct therapeutic interventions to treat SS and lupus. Therefore, the NZB/W F1 mouse is a powerful tool to understand the pathogenic mechanisms involved in SS related polyautoimmunity.

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