Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.

By Caroline E. Sutton, S. Lalor, C. Sweeney, Corinna F. Brereton, E. Lavelle, K. Mills. Immunity, 2009

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Interleukin-22: immunobiology and pathology (2015, background): “Interestingly, IL-22 production can be induced by IL-1β, independently of IL-23, although combined they act synergistically (55).”
Intestinal homeostasis and its breakdown in inflammatory bowel disease (2011, background): “In particular, γδ T cells can express the T H 17-associated transcription factors RORγt and the aryl hydrocarbon receptor (AHR), as well as the homing receptor CCR6, and can secrete IL-17 and IL-22 in response to IL-23 and IL-1&beta”
The IL-1 family: regulators of immunity (2010, background): “γδ T cells can make large quantities of IL-17 after stimulation with IL-1 and IL-23, and these cells can infiltrate the brain and have an important role in driving the development of EA”
Innate IL-17-producing cells: the sentinels of the immune system (2010, background): “Innate IL-17-producing cells can also interact with memory cells during chronic inflammatio”
Bleomycin and IL-1β–mediated pulmonary fibrosis is IL-17A dependent (2010, background): “Similarly, IL1 can stimulate IL17A production (Sutton et al., 2009), and IL1 is a critical mediator of pulmonary fibrosis (Gasse et al., 2007).”