The standard model of desiccating environmental stress was used to induce immune-driven dry eye disease (20 (link), 26 (link)–28 (link)). Briefly, mice were placed in cages with a perforated screen walls and exposed to continuous airflow from fans in a low humidity (20–30%) cubicle. Lacrimal gland function was inhibited by injection with scopolamine hydrobromide (0.1 mL of 10 mg/mL, formulated in sterile saline; Sigma-Aldrich Corp., St Louis, MO) for 3 or 5 consecutive days, and a reduced dose (0.1 mL of 5 mg/mL) for 10 days, respectively. Scopolamine hydrobromide injections were performed three times per day (9 AM, 2 PM, and 7 PM), subcutaneously into alternating hindquarters of mice. Age- and sex-matched untreated mice housed in standard animal facility environment served as healthy controls. In selected experiments mice were rendered neutropenic (29 (link), 30 (link)) by i.p. injection of purified anti-Ly6g (1A8 clone, 200 μg, BD PharMingen) 24 h prior to starting desiccating stress (1st injection) and 2 days after induction of dry eye disease (2nd injection). Control mice received the same dose of serum type IgG. Selected mice were treated topically (100 ng, tid) and systemically (1 μg, qd) with LXA4 (Cayman Chemical, Ann Arbor, MI) or sterile saline alone (PBS, ph 7.4) throughout 10 days of desiccating stress. Ethanol from LXA4 stock solution was rapidly removed under gentle stream of nitrogen and autacoids immediately resuspended in sterile saline and applied to the eye (5μl/drop) (31 (link), 32 (link)). Corneas with complete limbus, lacrimal glands and cervical draining lymph nodes were surgical excised with sterile instruments, and cleaned in ice-cold sterile phosphate-buffered saline under a dissecting microscope. Lacrimal glands were weighed and each draining lymph node was extracted with the diameter controlled 1.8–2.0 mm. Isolated tissues were either snap frozen for RNA/lipidomic/myeloperoxidase analyses or immediately processed for flow cytometry/ immunohistochemistry.