Pigmentary disorders: immune pathway in vitiligo: practice question

A Dermatology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Dermatology · Pigmentary disorders: immune pathway in vitiligo

Sample item

Topical ruxolitinib can repigment active nonsegmental vitiligo. Which pathway in the disease does it block?

ATNF-alpha signalling that causes keratinocyte apoptosisBIL-17A signalling that recruits neutrophils to the epidermisCInterferon-gamma signalling through JAK-STAT, with CXCL10 recruiting CD8 T cellsDIL-4 and IL-13 signalling from Th2 cells driving IgE

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

C. Interferon-gamma signalling through JAK-STAT, with CXCL10 recruiting CD8 T cells

In vitiligo, autoreactive CD8 T cells destroy melanocytes. Interferon-gamma acting through JAK1/2 and STAT1 induces keratinocytes to secrete CXCL9 and CXCL10, which recruit more T cells. JAK inhibitors interrupt this loop and, with phototherapy, can repigment lesions.

Option by option

A. TNF-alpha signalling that causes keratinocyte apoptosis
TNF-alpha has a limited role in vitiligo, and anti-TNF agents are not effective treatment.
B. IL-17A signalling that recruits neutrophils to the epidermis
IL-17A signalling is central to psoriasis and is not the main driver of melanocyte loss.
C. Interferon-gamma signalling through JAK-STAT, with CXCL10 recruiting CD8 T cells (correct)
Correct. The interferon-gamma, JAK-STAT and CXCL10 loop sustains CD8 T cell attack on melanocytes.
D. IL-4 and IL-13 signalling from Th2 cells driving IgE
IL-4 and IL-13 signalling drives atopic dermatitis rather than vitiligo.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

Questions about this Dermatology question

What is the answer to this Dermatology question?

The best answer is C, Interferon-gamma signalling through JAK-STAT, with CXCL10 recruiting CD8 T cells. In vitiligo, autoreactive CD8 T cells destroy melanocytes.

Why is "TNF-alpha signalling that causes keratinocyte apoptosis" not the answer?

TNF-alpha has a limited role in vitiligo, and anti-TNF agents are not effective treatment.

Why is "IL-17A signalling that recruits neutrophils to the epidermis" not the answer?

IL-17A signalling is central to psoriasis and is not the main driver of melanocyte loss.

Why is "IL-4 and IL-13 signalling from Th2 cells driving IgE" not the answer?

IL-4 and IL-13 signalling drives atopic dermatitis rather than vitiligo.

What concept does this question test?

It tests Pigmentary disorders: immune pathway in vitiligo in Dermatology. Interferon-gamma acting through JAK1/2 and STAT1 induces keratinocytes to secrete CXCL9 and CXCL10, which recruit more T cells. JAK inhibitors interrupt this loop and, with phototherapy, can repigment lesions.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Pigmentary disorders: immune pathway in vitiligo?

Learn each condition by its primary lesion, site and signature sign. Then use the flashcards and the other Dermatology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.