TYPE 2 IMMUNITY FAVORS CORNEAL NEUROREGENERATION IN A CORNEAL CHEMICAL INJURY MODEL

CERNUTTO A; PIZZANO, MANUELA; VEREERTBRUGGHEN, ALEXIA; SABBIONE F; KEITELMAN I; SHIROMIZU CM; VERA AGUILAR, DOUGLAS; FEDERICO FUENTES; GIORDANO , M; TREVANI A; GALLETTI J

San Luis

Congreso; LXXI Reunión Anual de la Sociedad Argentina de Inmunología (SAI); 2023

Introduction: Corneal nerves are affected by poorly understood mechanisms ininflammatory ocular surface disorders, causing ocular pain. We have shown thattype 1 immunity, and more specifically, Th1 CD4+ T cells foster cornealneuropathy. Since type 2 immune responses promote neural recovery in thebrain, here we hypothesized that type 2 immunity in the ocular surface could favorcorneal nerve regeneration.Methods: OTII [transgenic for an ovalbumin (OVA)-specific T cell receptor] andBalb/c mice were immunized with 25 μg OVA+5 μg alum (2 i.p. doses, days -14and -7) to induce type 2 immunity; then, corneal damage was induced from days-6 to 0 by instilling 0.1% benzalkonium chloride (BAK), a commonly used eyedrop preservative with known neurotoxicity; and finally, either OVA or saline wereinstilled daily in both eyes for 2-3 weeks. Corneal neurodegeneration wasassessed by functional assays [corneal mechanosensitivity (CMS), capsaicinsensitivity, eye closing ratio) and confocal microscopy (βIII tubulin staining).Results: On day 1 after BAK exposure, both control and immunized OTII micehad comparable corneal epitheliopathy (staining MFI: 10.48 vs 12.37, p=0.15)and CMS (-59±7% vs -56±8%, p=0.93). Compared to saline, ocular OVAchallenge over 20 days accelerated CMS recovery (p