dysregulation of AID—whether by deficiency or overexpression—has profound implications for autoimmune disease pathogenesis, immune tolerance &genomic stability, linking chronic inflammation, autoimmunity & cancer risk through its central role in #Bcellbiology & DNA editing processes

Dysregulation of AID, either through deficiency or overexpression, can disrupt these processes and contribute to the development of autoimmune diseases .

The precise mechanisms of its action and regulation, as well as its broader roles in epigenetic modulation & tumorigenesis . AID also plays a role in central and peripheral B cell tolerance, including the removal of polyreactive B cells during precursor stages

AID is a central enzyme in antibody maturation and immune diversification, but its mutagenic potential and off-target effects make it a critical factor in genomic instability & cancer development, especially under conditions of chronic inflammation or dysregulation.

a process essential for antibody diversification through somatic hypermutation (SHM), class switch recombination (CSR), and gene conversion (GC) in germinal center #Bcells. AID is normally expressed in activated B cells within germinal centers and is tightly regulated to prevent unwanted mutations .

Congrats ❣️

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- Disruption of microclots➡️ Potential reduction in chronic inflammation and autoimmunity

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- Entrapment of proteins ➡️ Potential induction of autoantibodies
- Targeting fibrin inflammatory domains➡️ Reduced microglial activation & thromboinflammation

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- Resistance to fibrinolysis➡️Persistent inflammation and hypoxia

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Summary The Studies on 🔑 Effects of Targeting Amyloid Fibrils on Immune Response in #LongCOVID in this🧵
- Amyloid microclot formation ➡️ Entrapment of inflammatory molecules & antibodies
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However, clinical evidence in humans is still limited & further research is needed to determine the efficacy & safety of these targeted therapies

inhibiting spike-fibrin interactions, or using immunotherapies may improve outcomes by reducing chronic inflammation, autoantibody production & microvascular dysfunction .

& neurological manifestations of COVID ,LC The persistence of spike protein & amyloid microclots in LC patients is linked to ongoing symptoms & impaired quality of life
. Targeting these pathological features either by promoting fibrin resolution,

However, translation of these findings to human pathology remains uncertain, as the complexity of hypercoagulation and neuroinflammation in humans may involve additional factors . #Fibrinimmunotherapy has been proposed as a strategy to ⏬️ systemic thromboinflammation

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🐁 model studies have demonstrated that targeting the inflammatory domain of fibrin with monoclonal antibodies can protect against microglial activation in 🧠 & thromboinflammation in the lung, indicating a potential therapeutic avenue

The interaction between the spike protein and fibrin is proposed as a fundamental driver of clotting pathology in both acute and long COVID, suggesting that therapies targeting either the spike protein or the abnormal amyloid fibrin itself may be beneficial

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