Interconnected skin cells showing ADAMTSL5 proteins and inflammatory pathways in psoriasis.

Unlocking Psoriasis: How a New Skin Protein Discovery Could Revolutionize Treatment

Mira Elwood in Health & Wellness August 2025 • 5 min read.

"Is ADAMTSL5 the Key to Calming Inflammation and Improving Skin Health? Uncover the latest research and its potential impact on psoriasis management."

Psoriasis is a chronic inflammatory skin condition affecting millions worldwide. Characterized by thick, scaly plaques, psoriasis not only impacts physical health but also significantly affects mental well-being. While current treatments offer relief, a complete cure remains elusive, driving ongoing research into the underlying mechanisms of the disease.

Traditionally, psoriasis has been understood as a condition driven by immune cells, particularly T cells, infiltrating the skin and causing inflammation. These T cells, along with various inflammatory molecules, contribute to the rapid turnover of skin cells, leading to the characteristic plaques. Recent studies have begun to explore the role of specific proteins and antigens that trigger these immune responses.

One such protein, ADAMTSL5 (A Disintegrin-like and Metalloprotease domain containing Thrombospondin Type 1 motif-like 5), has recently emerged as a potential key player in psoriasis. Initially identified in melanocytes (pigment-producing cells), a new study suggests that ADAMTSL5's role extends far beyond these cells, opening up new avenues for understanding and treating this complex condition.

ADAMTSL5: More Than Just a Melanocyte Protein

Interconnected skin cells showing ADAMTSL5 proteins and inflammatory pathways in psoriasis.

The original research focused on ADAMTSL5 because it was found to be produced by melanocytes and could activate IL-17-producing T cells, which are known to be central to the inflammatory process in psoriasis. However, a curious disconnect existed: melanocytes reside at the base of the epidermis, while T-cell infiltrates are scattered throughout the epidermis and heavily concentrated in the dermis. This raised the question: Could ADAMTSL5 be present in other skin cells as well?

To investigate this, researchers used immunohistochemistry to examine skin biopsies from psoriasis patients. They used three different commercially available antibodies to target ADAMTSL5. The results confirmed that ADAMTSL5 was indeed present in melanocytes. But, surprisingly, they also found strong expression of ADAMTSL5 in keratinocytes (the primary cells of the epidermis), as well as scattered expression in some dermal blood vessels and other dermal cells. This broader distribution suggests a more complex role for ADAMTSL5 in psoriasis than previously thought.

This discovery has several important implications:

Wider Impact: ADAMTSL5 may directly influence the inflammatory processes within the epidermis and dermis due to its presence in keratinocytes and dermal cells.
T-Cell Activation: The protein could be activating T-cells in more locations than just near melanocytes, explaining the widespread infiltration pattern seen in psoriasis.
New Treatment Targets: Targeting ADAMTSL5 in keratinocytes and dermal cells could provide new therapeutic strategies to reduce inflammation and slow down skin cell turnover.
Diagnostic Potential: Assessing ADAMTSL5 levels in different skin cell types could offer a more detailed understanding of psoriasis severity and individual patient responses to treatment.

The research team also noted that the expression pattern of ADAMTSL5 closely mirrored the infiltration pattern of T-cells and dendritic cells in psoriasis lesions. Dendritic cells are immune cells that capture and present antigens to T-cells, initiating an immune response. This close spatial relationship suggests that ADAMTSL5 might be involved in a complex interplay between keratinocytes, dendritic cells, and T-cells, driving the chronic inflammation characteristic of psoriasis. It’s like discovering that a key ingredient in a recipe is not only used in the main dish but also subtly flavors the side dishes, impacting the overall taste experience.

The Future of Psoriasis Treatment: Targeting ADAMTSL5

The discovery of ADAMTSL5 expression in keratinocytes and dermal cells significantly broadens our understanding of its role in psoriasis. While further research is needed to fully elucidate the mechanisms by which ADAMTSL5 contributes to the disease, this finding opens exciting new avenues for therapeutic intervention. By targeting ADAMTSL5 in these additional cell types, researchers may be able to develop more effective treatments that address the root causes of psoriasis, offering hope for improved management and long-term relief for those affected by this challenging condition. It’s a bit like finding a hidden room in a house – it changes the whole layout and suggests new possibilities for how the space can be used.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.4172/2376-0427.1000244, Alternate LINK

Title: Cutaneous Expression Of A Disintegrin-Like And Metalloprotease Domain Containing Thrombospondin Type 1 Motif-Like 5 (Adamtsl5) In Psoriasis Goes Beyond Melanocytes

Subject: General Medicine

Journal: Journal of Pigmentary Disorders

Publisher: OMICS Publishing Group

Authors: Kathleen M Bonifacio, Norma Kunjravia, James G Krueger, Judilyn Fuentes Duculan

Published: 2016-01-01

Everything You Need To Know

What is ADAMTSL5 and why is it important in the context of psoriasis?

ADAMTSL5, short for A Disintegrin-like and Metalloprotease domain containing Thrombospondin Type 1 motif-like 5, is a protein. Initial research focused on ADAMTSL5 because it was found to be produced by melanocytes, and could activate IL-17-producing T cells central to the inflammatory process in psoriasis. Further investigation revealed its presence in keratinocytes and dermal cells. This broader distribution suggests a more complex role for ADAMTSL5 in psoriasis than previously thought.

How might targeting ADAMTSL5 change the future of psoriasis treatment?

The discovery of ADAMTSL5 expression in keratinocytes and dermal cells significantly broadens our understanding of its role in psoriasis. Targeting ADAMTSL5 in these additional cell types may lead to the development of more effective treatments. These treatments could address the root causes of psoriasis, offering hope for improved management and long-term relief. Diagnostic potential exists in assessing ADAMTSL5 levels in different skin cell types for a more detailed understanding of psoriasis severity and individual patient responses to treatment.

What are the specific implications of finding ADAMTSL5 in both keratinocytes and dermal cells?

The research indicates that ADAMTSL5 may directly influence inflammatory processes within the epidermis and dermis due to its presence in keratinocytes and dermal cells. It could also be activating T-cells in more locations than just near melanocytes, explaining the widespread infiltration pattern seen in psoriasis lesions. Furthermore, the expression pattern of ADAMTSL5 closely mirrored the infiltration pattern of T-cells and dendritic cells in psoriasis lesions, suggesting a complex interplay between keratinocytes, dendritic cells, and T-cells, driving the chronic inflammation.

How did researchers discover the presence of ADAMTSL5 in different skin cells, and what tools did they use?

The study used immunohistochemistry to examine skin biopsies from psoriasis patients, employing three different commercially available antibodies to target ADAMTSL5. Researchers confirmed ADAMTSL5 presence in melanocytes, but also found strong expression in keratinocytes (the primary cells of the epidermis), as well as scattered expression in some dermal blood vessels and other dermal cells. This broader distribution suggests a more complex role for ADAMTSL5.

How does the role of T-cells relate to ADAMTSL5 in the development of psoriasis?

Psoriasis is understood as a condition driven by immune cells, particularly T cells, infiltrating the skin and causing inflammation. These T cells, along with various inflammatory molecules, contribute to the rapid turnover of skin cells, leading to thick, scaly plaques. The recent discovery of ADAMTSL5 as a potential key player is due to its impact on T-cell activation. The expression pattern of ADAMTSL5 closely mirrored the infiltration pattern of T-cells and dendritic cells in psoriasis lesions. This close spatial relationship suggests that ADAMTSL5 might be involved in a complex interplay between keratinocytes, dendritic cells, and T-cells, driving the chronic inflammation characteristic of psoriasis.