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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Rapid monocyte infiltration following retinal detachment is dependent on non-canonical IL6 signaling through gp130

Fig. 4

Model summary of intraocular IL6 and gp130 signaling. a One day after RD, retina secretes CCL2, sICAM-1 and TIMP-1. Bone marrow derived-monocytes are recruited into the vitreous. Active monocytes upregulate p-STAT3 and p-Erk1/2. However, anti-gp130 treatment inhibits CCL2 secretion and monocyte recruitment, by strengthening p-STAT3 and downregulating p-Erk1/2 in vitreous monocytes after RD. IL6 knockout mice inhibit CCL2 and TIMP-1 secretion, weaken p-STAT3 and p-Erk1/2 activation after RD. b Seven cytokines signal via gp130, but most of the them and their co-receptors have very weak or undetectable expression (shown by dotted line) in mouse retina, including IL6 and receptor IL6Rα. In the retina, gp130 only signals through IL11/IL11Rα (shown by solid line) but IL11 is not changed after RD. This can explain why there was no IL6/IL6Rα protein expression in retina and why there were no significant changes of gp130, p-STAT3, p-Akt and p-Erk1/2 in retina after RD in our study. Despite high IL6 in vitreous (secreted by monocytes), the retinal IL6/IL6Rα signaling is silent. Therefore, anti-gp130, not anti-IL6 or anti-IL6Rα, may be beneficial to retina, by intervening early inflammation after RD

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