The complex alteration in the network of IL-17-type cytokines in patients with hereditary angioedema

Gabriella Misiano, Giuseppina Colonna Romano, Vito Michele Rosario Muggeo, Mariangela Lo Pizzo, Mariangela Lo Pizzo, Francesco Arcoleo, Enrico Cillari, Enrico Cillari, Salvatore Milano

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5 Citations (Scopus)


Hereditary angioedema (HAE) is a rare autosomic-dominant disorder characterized by a deficiency of C1 esterase inhibitor which causes episodic swellings of subcutaneous tissues, bowel walls and upper airways that are disabling and potentially life-threatening. We evaluated n = 17 patients with confirmed HAE diagnosis during attack and remission state and n = 19 healthy subjects. The samples were tested for a panel of IL (Interleukin)-17-type cytokines (IL-1β, IL-6, IL-10, granulocyte–macrophage colony stimulating factor (GM-CSF), IL-17, IL-21, IL-22, IL-23) and transforming growth factor-beta (TGF-β) subtypes. Data indicate that there are variations of cytokine levels in HAE subjects comparing the condition during the crisis respect to the value in the remission phase, in particular type 17 signature cytokines are increased, whereas IL-23 is unmodified and TGF-β3 is significantly reduced. When comparing healthy and HAE subjects in the remission state, we found a significant difference for IL-17, GM-CSF, IL-21, TGF-β1 and TGF-β2 cytokines. These results confirm and extend our previous findings indicating that in HAE there is operating an inflammatory activation process, which involves also T helper 17 (Th17) cytokines and TGF-β isoforms, associated with localized angioedema attacks and characterized by elevated bradykinin levels.
Original languageEnglish
Pages (from-to)355-361
Number of pages7
JournalClinical and Experimental Medicine
Publication statusPublished - 2018

All Science Journal Classification (ASJC) codes

  • General Biochemistry,Genetics and Molecular Biology


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