IL-36α (IL-1F6), IL-36β (IL-1F8) and IL-36γ (IL-1F9) are members of the IL-1 cytokine family that bind to IL-36R (IL-1Rrp2) and IL-1RAcP, activating similar intracellular signals as IL-1 and are inhibited by IL-36Ra (1). The expression of IL-36 cytokines occurs mainly in the lung and skin and can be derived from diverse epithelial cell types including keratinocytes, bronchial epithelium as well as macrophages, monocytes and different T cell subsets. IL-36γ expression is significantly induced upon TLR stimulation and induced in bronchial epithelium exposed to inflammatory stimuli suggesting that these proteins are involved in first-line defences against microorganisms (1,2). IL-36 family members induce the production of pro-inflammatory cytokines, including IL-12, IL-1β, IL-6, TNF-α and IL-23, thus promoting neutrophil influx, dendritic cell (DC) activation, polarization of T helper type 1 (Th1) and IL-17-producing T cells (αβ T cells and γδ T cells) and keratinocyte proliferation (1). The IL-36 cytokines may represent potential targets for immune-mediated inflammatory conditions or, alternatively, could be used as adjuvants in vaccination. Induction of IL-36γ in macrophages upon M. tuberculosis infection and its role in the release of antimicrobial peptides has been proposed (2). IL-36γ is also induced in the lung in various models of asthma and can be produced by bronchial epithelial cells in response to viral infection, smoke or inflammatory cytokines and plays an important role in asthmatic pulmonary inflammation (3). IL-36γ might be a potential biomarker of Inflammatory Bowel Disease (4,5), and is highly expressed in inflamed skin from psoriasis patients and in Allergic Contact Dermatitis (6). IL-36γ serum levels are enhanced and correlate to psoriasis severity and response to treatment with anti-TNF (7).
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