T helper (Th)17 radiation-induced hidradenitis suppurativa

To the Editor: We read with interest the case report describing the development of hidradenitis suppurativa (HS) lesions after radiation treatment in a patient with uterine adenocarcinoma.¹ The authors provided several thoughts on the possible mechanism behind radiation-induced HS. The purpose of this letter is to provide additional insight about the likely immunologic mechanisms behind radiation-induced HS. The reported case is an example of an abscopal-like effect² sharing adenocarcinoma antigens to antigens of apocrine glands of the groin. Abscopal effect is an immune-mediated phenomenon that has been heavily discussed in metastatic melanoma, whereby there is regression of nonirradiated metastatic lesions after irradiation of a distant melanoma tumor location.3, 4 Abscopal effects were also recently reported in advanced melanoma patients after immunotherapy, highlighting the therapeutic implications of this phenomenon.⁵

As the authors point out, apoptosis can be induced by irradiation.¹ It is likely that apoptotic uterine adenocarcinoma cells result in T-cell cross priming after radiation⁶ and activate Th17 subset. A recent article points out that Th17 is an important subset in the immunopathogenesis of HS,7, 8 like it is in psoriasis.⁹ This case and the article by Matusiak et al⁷ make a strong case that HS, like psoriasis, is an autoimmune disease with Th17 and the attendant polymorphonuclear leukocytes involved. Oppman et al¹⁰ identified the p19 third subunit of interleukin (IL)-12, and designated it as IL-23. This finding predicted the potential for treating psoriasis with anti–IL-12 ustekinumab and anti–IL-23 (guselkumab). This case of radiation-induced HS is likely to predict a positive outcome with clinical trials for HS with ustekinumab (IL-12 antagonist),¹¹ secukinumab (IL-17 antagonist),¹² and guselkumab (IL-23 antagonist).¹³