A Multi-Omics Perspective of Vitiligo

Featuring Model Rosalinda 

Photography by Florence Piel

What is Vitiligo?

Vitiligo is a condition in which the immune system mistakenly attacks the cells that produce skin pigment (melanocytes). Leading to white patches on the skin. Vitiligo affects 1% of people worldwide.

ALL ages,

ALL  backgrounds

AND skin tones.

(even dogs, horses, and cats get vitligo)

What is Multi-Omics?

By “multi-omics”, we are referring to an integrated biological approach that combines all the “omics” information layers:

Genomics ⟶ DNA

Transcriptomics ⟶ RNA

Proteomics ⟶ Proteins

Metabolomics ⟶ Metabolites i.e. Metabolism

In the next few paragraphs we will be asking and answering questions from each biological omic presepctive...

Genomics in Vitiligo

Are some people genetically predisposed to vitiligo? 

Yes. Around 15–30% of vitiligo cases show familial clustering, indicating a genetic predisposition. Small DNA differences can raise the risk by affecting the immune system, but they don’t cause vitiligo by themselves.

Is vitiligo caused by a single genetic mutation or is it polygenic?

Vitiligo is polygenic.This means that there is no single “vitiligo gene”. Instead it is several genetic variants working together that shape how the immune system behaves.

Does vitiligo share risk genes with other autoimmune pathways?

Yes (very strongly). Many vitiligo-associated genetic variants are also linked to other autoimmune diseases, including Type 1 diabetes, Rheumatoid arthritis, & Autoimmune thyroid disease. That is why Vitiligo is considered a immune related

condition (not just a skin disorder)

Transcriptomics in Vitiligo

Genomics asks about predisposition,

transcriptomics asks about process

Which genes are active right now?

Transcriptomics shows increased activity of immune and inflammatory genes, especially in:

• Immune cells (T-cells)

• Skin cells (Keratinocytes)

• Pigment producing cells (Melanocytes)

At the same time, genes important for melanocyte survival and function become less active.

When does the immune response begin?

Transcriptomic changes appear before visible pigment loss, meaning vitiligo begins as a silent immune process long before it becomes visible on the skin.

Proteomics in Vitiligo

Transcriptomics asks about process,

Proteomics asks about action

Which proteins are doing the damage?

• Immune signaling proteins intensify the immune response

• Attack proteins damage pigment-producing cells

• Protective proteins fail to prevent that damage

Which proteins are present, active, absent?

Not all RNA transcripts turn into proteins, therefore soley studing transcriptomics isn’t enough. We need to see which immune, inflammatory, and stress-related proteins are produced/active in vitiligo AND which ones are absent!

Metabolomics in Vitiligo

Proteomics asks about action,

Metabolomics asks about outcome

What is the chemical environment of the cell?

Metabolomics is looking at the chemical envionrment inside of the cell. Factors like:

• Cellular stress

• Energy use

• Oxidative damage

In vitiligo, this shows whether skin cells are surviving in a harmful chemical environment.

How does metabolism shift during disease?

As vitiligo develops, the chemical balance inside skin cells changes in ways that make pigment cells more fragile. Essentially, metabolism reflects the final outcome of genetic risk, immune signals, protein damage and their downstream consequences.

How does a multi-omics view change how you think about Vitiligo?