Scholarlink

<p>Acne vulgaris is a chronic inflammatory skin condition with a multifactorial pathogenesis involving follicular hyperkeratinization, sebaceous gland dysregulation, microbial dysbiosis—particularly involving <i>Cutibacterium acnes</i> and <i>Staphylococcus epidermidis</i>—and complex immune-mediated mechanisms, on which T helper cell 1 (T<sub>h</sub>1) and T<sub>h</sub>17 pathways are central players. This evolving understanding has led to the exploration of biologic therapies targeting cytokines such as tumor necrosis factor-alpha (TNFα), interleukin (IL)-1, IL-17, and IL-23. However, clinical trials to date have not demonstrated efficacy of biologics in moderate to severe acne. In contrast, some case reports and studies suggest clinical improvement with TNFα and IL-17A inhibitors in severe, treatment-resistant acne, although these presentations often overlap with hidradenitis suppurativa (HS), raising questions about diagnosis and underlying disease mechanisms. Furthermore, in various monogenic autoinflammatory syndromes where “acne-like” lesions are part of the clinical spectrum, biologic therapies have shown effectiveness. These observations suggest that in such contexts, the lesions may reflect HS or HS-like pathology rather than true acne, potentially explaining the therapeutic benefit of biologicals in this context. This review synthesizes current insights into the immunopathogenesis of acne and critically evaluates the rationale, evidence, and limitations of biologic therapy in its treatment. While biologics hold promise in defined inflammatory dermatoses, their role in the management of acne vulgaris remains unproven and may be limited to specific phenotypes that overlap with autoinflammatory or HS-related conditions.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Is There a Place for Biologics in Acne?

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月5日

查看全文
  • Lajos Kemény,
  • Döníz Degovics,
  • Kornélia Szabó

摘要

Acne vulgaris is a chronic inflammatory skin condition with a multifactorial pathogenesis involving follicular hyperkeratinization, sebaceous gland dysregulation, microbial dysbiosis—particularly involving Cutibacterium acnes and Staphylococcus epidermidis—and complex immune-mediated mechanisms, on which T helper cell 1 (Th1) and Th17 pathways are central players. This evolving understanding has led to the exploration of biologic therapies targeting cytokines such as tumor necrosis factor-alpha (TNFα), interleukin (IL)-1, IL-17, and IL-23. However, clinical trials to date have not demonstrated efficacy of biologics in moderate to severe acne. In contrast, some case reports and studies suggest clinical improvement with TNFα and IL-17A inhibitors in severe, treatment-resistant acne, although these presentations often overlap with hidradenitis suppurativa (HS), raising questions about diagnosis and underlying disease mechanisms. Furthermore, in various monogenic autoinflammatory syndromes where “acne-like” lesions are part of the clinical spectrum, biologic therapies have shown effectiveness. These observations suggest that in such contexts, the lesions may reflect HS or HS-like pathology rather than true acne, potentially explaining the therapeutic benefit of biologicals in this context. This review synthesizes current insights into the immunopathogenesis of acne and critically evaluates the rationale, evidence, and limitations of biologic therapy in its treatment. While biologics hold promise in defined inflammatory dermatoses, their role in the management of acne vulgaris remains unproven and may be limited to specific phenotypes that overlap with autoinflammatory or HS-related conditions.