Fig. 1: Clinical and histopathological features of six PRP patients with KRT32 mutations. | Nature Communications

Fig. 1: Clinical and histopathological features of six PRP patients with KRT32 mutations.

From: Loss-of-function mutations in Keratin 32 gene disrupt skin immune homeostasis in pityriasis rubra pilaris

Fig. 1

Photographs of cutaneous lesions and histological analysis of skin biopsy specimens from PRP patients with KRT32 mutations are presented. These patients manifested typical pathological characteristics of PRP, including widespread erythematous plaque coalescence, layered parakeratosis, absence of Munro microabscesses, alternating hyperkeratosis and parakeratosis, irregular thickening of the stratum spinosum, sparse lymphoid cell infiltration around superficial dermal blood vessels, and hair follicular plugging (labeled by black arrows). Each group of H&E-stained histological images are captured at two magnification levels – 100× (left) and 200× (right), and the mutation site is presented below the respective images. The process of producing these representative H&E-stained histological images was repeated, yielding similar results for all the 3 slides (n = 3) per patient.

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