Corneal allograft rejection can be seen in some patients after corneal transplantation. The present study intends to investigate whether JAK2 gene knockout affects corneal allograft rejection through regulation of dendritic cells (DCs)-induced T cell immune tolerance. In order to identify the target gene related to corneal allograft rejection, high-throughput mRNA sequencing and bioinformatics analysis were performed. JAK2 knockout mice were constructed and subjected to corneal allograft transplantation. The incidence of immune rejection was observed, the percentage of CD4⁺ T cells was detected, and the expression of Th1 cytokine interferon γ (IFN-γ) was determined. Flow cytometry and ELISA were performed to analyze the effects of JAK2 gene knockout on bone marrow-derived DCs (BMDCs). JAK2 was the target gene related to corneal allograft rejection. JAK2 gene knockout contributed to significantly prolonged survival time of corneal grafts in mice and inhibited corneal allograft rejection. The in vitro cell experiment further confirmed that JAK2 gene knockout contributed to the inactivation of CD4⁺ T cells and induced IFN-γ expression, accompanied by inhibition of DC immune function, development, maturation, and secretion of inflammatory cytokines. Collectively, JAK2 gene knockout inactivates CD4⁺ T cells to decrease IFN-γ expression, as well as inhibits DC development, maturation, and secretion of inflammatory cytokines, thereby reducing corneal allograft rejection.

To investigate the clinical pathways via which the glaucomatous optic nerve damage (GOND) occurred in cases with glaucomatocyclitic crisis (also called Posner-Schlossman syndrome, PSS). A retrospective study was conducted, 59 PSS patients with confirmed GOND were screened out from 190 PSS cases and followed up for a period of 5 ± 3.3 years. Clinical data were retrospectively analyzed systematically and dynamically, including intraocular pressure and its dynamic change, appearance of fundus, visual field and the state of anterior chamber angle in initial and later period during the episodes and intermission of PSS. Based on the clinical data, a classification and standard for the clinical pathways of GOND were established, and the clinical pathway of GOND in each patient was classified accordingly. There are at least 4 clinical pathways of GOND in PSS patients, namely: Type A: GOND was simply caused by the accumulation effect of high IOP during many attacks of PSS itself. Type B: GOND was resulted from the combined action of PSS itself and another type of secondary open-angle glaucoma. The recurrent inflammation during the episodes of PSS damaged the trabecular meshwork, which can cause elevation of IOP during the intermission of PSS. Type C: PSS combined with primary open angle glaucoma (POAG). Type D: PSS combined with primary angle-closure glaucoma (PACG). Base on the clinical gateways of GOND classification above, the cases of type A, B, C, and D were 27, 6, 19, and 7 respectively. The staging of visual field damage in cases with GOND from different clinical pathways showed a significant difference (Person chi-square χ² test, χ² = 7.211, P = .007). There are at least 4 clinical pathways of GOND in PSS patients, and each clinical pathway corresponds to different clinical features and different treatment principles. It is extremely important to correctly discriminate the pathways of GOND in PSS patients.