Aisha Weththasingha

A literature review of how monoclonal antibodies treat lesional skin in atopic dermatitis and a proposal of an anti-inflammatory therapy approach targeting CCL22’s binding to CCR4

Started Oct. 23, 2023

Abstract or project description

Inflammation and lesional skin in patients with atopic dermatitis (AD) results from an inflammatory pathway and chemotactic signaling. Once T helper 2 (Th2) cells, a type of T lymphocyte, produce and activate certain cytokines, inflammation is stimulated. Inflammation is further developed and intensified by the presence of chemokines such as C-C motif chemokine ligand 22 (CCL22) and C-C motif chemokine ligand 17 (CCL17) binding to their receptor, C-C motif chemokine receptor 4 (CCR4). Once bound, these chemokines direct inflammatory cytokines to existing sites of inflammation, further developing and intensifying inflammation and lesional skin.

Current treatments using monoclonal antibodies (MAs) include dupilumab and tralokinumab,both of which target interleukins. They have both shown to be effectiveas targeted therapies but still fall short in a few specific areas. Past research on the efficacy of inhibiting CCR4 has been conducted and used to create other monoclonal antibodies such as mogamulizumab. Mogamulizumab is a monoclonal antibody created to target CCR4 and prevent inflammation in another inflammatory disease. It has proven effective in its design. Multiple other monoclonal antibodies have also been designed to target CCR4 to treat inflammation in other inflammatory diseases that are not atopic dermatitis. They have proven to be efficient in relieving inflammation or inflammatory responses.

Since the inhibition of CCR4 has proven to work well for other inflammatory diseases, it is possible that using monoclonal antibodies to bind to CCR4, preventing CCL22 from binding, may prove to be another effective treatment for inflammation and lesional skin in patients with atopic dermatitis.