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Factor VIII Infusion, Dosing and Administration for Hemophilia A

Immune Pathways Driving T Cell Inflammation in Atopic Dermatitis

Atopic dermatitis (AD) is a complex, biologically heterogeneous disease defined by contributions from multiple distinct inflammatory pathways.^1,2 In addition to the well characterized role of type 2 inflammation (and Th2 cells) in the development of atopic dermatitis, the Th17, Th22 and Th1 immune axes also contribute to inflammation caused by T cell dysregulation in AD.^1,3 T cell inflammation in atopic dermatitis involves a broad immune response, where cytokines are part of a larger T-cell mediated cycle of immune imbalance.^2,3

Gaucher Disease Therapy and Management

Gaucher Disease Pathophysiology

Gaucher Disease Genetics and Inheritance

The Role of OX40L/OX40R in Atopic Dermatitis (AD)

Atopic dermatitis (AD) is a chronic inflammatory heterogenous skin condition marked by immune dysregulation and impaired skin barrier function.^1,2 For healthcare professionals seeking to understand the immunologic drivers of AD, the OX40L signaling axis has emerged as a key pathway involved in T-cell activation and chronic inflammation.^2,3 

Systemic and Long-Term Atopic Dermatitis (AD) Treatment

Atopic dermatitis (AD) is a chronic inflammatory condition caused by complex underlying pathophysiology, driven by genetic, immunologic and environmental factors and triggers that collectively disrupt the epidermis.^1-3 Despite the range of treatment options available, patients continue to experience fluctuations in disease activity due to the heterogeneity of AD.^4-6 There remains an unmet need to develop a deeper understanding of the diverse immune dysregulation profiles found in patients with AD and determine optimal treatment on a more personalized basis.^4,6

Understanding Type 2 and Non-Type 2 Inflammation in Atopic Dermatitis

Atopic dermatitis (AD) is a heterogenous disease defined by contributions from multiple distinct inflammatory pathways.¹ Although type 2 inflammation‘s role in AD pathogenesis is well-characterized, other non-type 2 T cell-mediated pathways also play a role in AD chronicity.^1,2 For healthcare professionals seeking to understand the diversity of immune signatures in their AD patients, looking beyond Th2 cytokines is essential.¹

Understanding the Burden of Moderate-to-Severe Atopic Dermatitis

Atopic dermatitis (AD) is a chronic, immune-mediated inflammatory disease that often begins in early infancy and persists into adulthood.^1-3 While symptoms such as the intense itch that disrupts the lives of patients are well known, AD also imposes a profound chronic ‘hidden burden’ that extends far beyond visible skin lesions, significantly impairing patients' mental health, relationships, and daily productivity.^1-11 This burden can be compounded by the treatment regimens themselves, which can be time-consuming, economically straining, and limited by low patient satisfaction and patient phobias of treatments and their side effects.^12-14