Following ischemia/reperfusion of the testis IL-1β expression is increased. Corresponding with the increase in IL-1β is an activation of JNK localized to endothelial cells in the testis. Two downstream transcription factors of JNK, ATF-2 and c-jun are also activated and are known to form a heterodimer and upregulate E-selectin expression. E-selectin expressed on the surface of endothelial cells aids in the recruitment of neutrophils to the testis. Once neutrophils are bound to endothelial cells they can transmigrate through the endothelial cells into the interstitium where they are poised to release factors such as reactive oxygen species or other cytokines. The source of IL-1β production after ischemia/reperfusion of the testis is currently unkown; however, Sertoli cells, Leydig cells, and interstitial macrophages are candidates.