MEDB21 - IMUNOLOGIA I - Seminário Psoríase

Summary

This presentation covers the mechanisms, effects, and treatments of psoriasis, a chronic autoimmune condition. It explores the role of genetic predisposition, environmental triggers, and immune responses, particularly the activation of T cells and the release of cytokines like TNF-alpha and IL-17. The immune system's two phases—initiation and maintenance—are discussed, emphasizing the role of dendritic cells and lymphocytes in the inflammation process. Treatment options, including immunobiological therapies targeting IL-23, TNF-alpha, and IL-17, are also explored, offering hope for patients with moderate to severe psoriasis. The focus is on understanding and managing the condition through targeted therapies.

Takeaways

• 😀 Psoriasis is a chronic autoimmune disease that involves both innate and adaptive immune responses.
• 😀 Genetic predisposition and environmental factors such as infections, stress, and medication usage trigger psoriasis in susceptible individuals.
• 😀 The immune mechanisms in psoriasis are divided into two phases: the initiation of the inflammatory response and its maintenance.
• 😀 The activation of immune cells like dendritic cells, neutrophils, and keratinocytes plays a significant role in the development of psoriasis lesions.
• 😀 Cytokines such as TNF-α, IL-1β, IL-6, IL-17, and IL-23 are critical in both initiating and maintaining the inflammatory response in psoriasis.
• 😀 IL-36 is a key cytokine involved in the inflammatory process of psoriasis and is overexpressed in the lesions.
• 😀 Psoriasis can result in systemic inflammation, leading to a higher risk of cardiovascular diseases due to the involvement of cytokines like TNF-α and IL-17.
• 😀 Immunobiological treatments, such as IL-23 inhibitors, TNF-α inhibitors, and IL-17 inhibitors, are effective for treating moderate to severe psoriasis.
• 😀 Other treatment options for psoriasis include topical steroids, phototherapy, and systemic therapies, with immunobiologicals being reserved for more severe cases.
• 😀 IL-23 plays a major role in the differentiation of T-cells, particularly Th17 cells, which contribute to the chronic inflammatory nature of psoriasis.
• 😀 Immunobiological drugs target specific cytokines involved in the disease process, reducing inflammation and controlling psoriasis symptoms.

Q & A

What is psoriasis and what are the main triggers?

Psoriasis is a chronic inflammatory skin disease that can be triggered by environmental factors such as infections, stress, alcohol consumption, and certain medications. Individuals with genetic predisposition are more susceptible to developing psoriasis.

How is psoriasis initiated in the body?

Psoriasis initiation begins when environmental factors like infections, skin trauma, and medication use trigger immune responses. These factors activate molecules that stimulate innate immune cells, such as dendritic cells, neutrophils, and keratinocytes, which start the inflammatory process.

What is the role of dendritic cells in psoriasis?

Dendritic cells are crucial in psoriasis as they bridge the innate and adaptive immune systems. They secrete pro-inflammatory cytokines such as TNF-alpha and IL-23, which activate T-helper cells (Th1, Th2, Th17) and initiate the inflammatory cascade in the skin.

What are the key cytokines involved in psoriasis inflammation?

The key cytokines involved in psoriasis inflammation include TNF-alpha, IL-17, IL-6, IL-23, and interferon-alpha. These cytokines promote immune cell activation, vascular changes, and keratinocyte proliferation, contributing to the skin lesions seen in psoriasis.

How does the adaptive immune system contribute to psoriasis?

The adaptive immune system, particularly T-helper cells (Th1, Th17), plays a significant role in the maintenance of psoriasis. These cells produce cytokines like TNF-alpha and IL-17, which sustain the inflammatory response and skin cell turnover, leading to the persistence of lesions.

What genetic mutations are linked to psoriasis?

Genetic mutations in pathways related to immune system activation, such as defects in the IL-36 receptor antagonist, are linked to the development of psoriasis. These mutations can cause an increase in inflammatory cytokine production and immune cell activation, contributing to disease progression.

What role does IL-36 play in psoriasis?

IL-36 is a pro-inflammatory cytokine that plays a central role in psoriasis. It activates immune responses in the skin by inducing the release of other inflammatory cytokines and chemokines, such as IL-1 and IL-17, further exacerbating the inflammatory cascade.

What are the treatment options for psoriasis?

Psoriasis treatments focus on alleviating symptoms and promoting well-being. These include topical therapies like corticosteroids, phototherapy (UVB), and systemic treatments like immunobiologics, which target specific immune pathways to reduce inflammation and control the disease.

What is the role of immunobiologic treatments in managing psoriasis?

Immunobiologic treatments are used for moderate to severe psoriasis, particularly in cases resistant to other therapies. These treatments target specific cytokines like IL-23, TNF-alpha, and IL-17, preventing their interaction with immune cells and reducing inflammation in the skin.

Can psoriasis lead to cardiovascular diseases?

Yes, psoriasis, particularly through the involvement of pro-inflammatory cytokines like TNF-alpha and IL-17, has been linked to an increased risk of cardiovascular diseases. This is particularly true for individuals with metabolic syndrome and chronic inflammation.