Welcome to the 13th International Congress on Autoimmunity interactive program

Displaying One Session

Date
Mon, 13.06.2022
Session Time
08:00 - 10:00
Room
ALEXANDRA TRIANTI
Session Type
PLENARY SESSIONS

WHAT’S NEW IN LUPUS NEPHRITIS THERAPY? (ID 902)

Date
Mon, 13.06.2022
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
08:00 - 08:30

IS039 - RA AND THE BRAIN (ID 903)

Date
Mon, 13.06.2022
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
08:30 - 09:00

Abstract

Abstract Body

Rheumatoid arthritis (RA) was initially described as an inflammatory and destructive disease of synovial joints. However, over the last 20 years increasing focus has been directed towards the effects of chronic systemic inflammation on other organ systems. It is now clear that inflammation plays an important negative role in the development of cardiovascular disease and that DMARDs can reduce this risk. More recent research has considered the increased risk of brain related pathology such as stroke along with pain, depression/anxiety and even cognitive function. It has also been suggested that RA provides a model system to explore the consequences of chronic inflammation of relevance to all populations. This may be true for cardiovascular disease and dementia.

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THE REPERTOIRE OF AUTOANTIBODIES IN CELIAC DISEASE: ANY NEW ONE? (ID 905)

Date
Mon, 13.06.2022
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
09:00 - 09:30

IS040 - THE AUTOIMMUNE TAUTOLOGY: AN UP-DATE (ID 906)

Date
Mon, 13.06.2022
Session Time
08:00 - 10:00
Session Type
PLENARY SESSIONS
Room
ALEXANDRA TRIANTI
Lecture Time
09:30 - 10:00

Abstract

Abstract Body

Autoimmune diseases (ADs) exhibit a wide range of phenotypes depending on the target organ, however, their physiopathological mechanisms are similar. The holistic approach to ADs is known as the autoimmune tautology hypothesis, which is supported by ten arguments. First, the female predominance. Second, shared subphenotypes. Third, polyautoimmunity. Fourth, coaggregation (familial autoimmunity). Fifth, the influence of age at onset on severity. Sixth, similar pathophysiology. Seventh, similar environmental agents influence their development (that is, autoimmune ecology). Eighth, common genetic polymorphism are associated factors. Ninth, ancestry plays an importnat role, mainly in admixed populations. Lastly, Similar medications are used to treat ADs. In this lecture, I will discuss the most recent evidence that supports the autoimmune tautology.

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