Application of MAGT1 small interfering RNA in preparation of medicine for treating uveitis

Abstract

The invention relates to the technical field of biological medicine, in particular to application of MAGT1 small interfering RNA in preparation of medicine for treating uveitis, the MAGT1 small interfering RNA is RNA for interfering and reducing the expression quantity of MAGT1, the MAGT1 small interfering RNA provided by the invention can efficiently knock down the expression quantity of MAGT1 protein, down-regulate the proportion of Th1 cells and Th17 cells in CD4 + T cells and up-regulate the proportion of Treg cells, and the MAGT1 small interfering RNA can be used for preparing medicine for treating uveitis. According to the present invention, with the application of the pharmaceutical composition, the inflammatory reaction of uveitis is relieved, especially the treatment effect on the Vogt-Salix babylonica original field syndrome is provided, the supplement is provided for the uveitis pathogenesis, and the new strategy is provided for the target treatment of the uveitis.

Description

TECHNICAL FIELD

[0001] The present application relates to the technical field of biological medicine, and particularly relates to application of MAGT1 small interfering RNA in preparation of a drug for treating uveitis. BACKGROUND

[0002] Uveitis is a major blinding eye disease worldwide, which is insidious in onset, often occurs in young adults, and has characteristics of repeated attacks and difficulty in radical cure. In developed countries, the number of blind people caused by uveitis accounts for 10% to 15% of the total number of blind people, and in developing countries, about 25% of irreversible blindness is caused by uveitis and its complications. Vogt-Koyanagi-Harada (VKH) syndrome is one of the most common types of uveitis in China, which is characterized by repeated bilateral granulomatous panuveitis, and is an autoimmune disease that can involve multiple systems such as the auditory system, central nervous system, skin and hair. If not treated in time or the treatment plan is wrong, it often leads to severe visual loss or even blindness, and VKH syndrome can also cause complications such as secondary cataract, secondary glaucoma and optic nerve damage, thereby causing irreversible visual loss or visual function damage in patients.

[0003] Current studies have shown that environment, genetics, immunity and other factors are involved in the occurrence and development of VKH syndrome, especially CD4 + T cell-mediated immune response plays an important role in the pathogenesis of the disease. Previous studies have shown that Th1, Th17 / Treg cell imbalance plays an important role in the occurrence of VKH syndrome, but the exact mechanism of Th1, Th17 / Treg cell imbalance in the pathogenesis of the disease is not completely clear. Therefore, exploring the key molecules and mechanisms of VKH syndrome has become a problem to be solved in the current research of the disease.

[0004] Minerals are a class of indispensable micronutrients for the human body, and the deficiency of minerals is closely related to the occurrence and development of many diseases, and minerals play a very important role in immune regulation. At present, the role and mechanism of minerals in VKH syndrome are still unclear, and there is no report. Further exploring the pathogenesis of VKH syndrome by taking minerals as the research target and revealing the key molecules are expected to further improve the treatment effect, treatment safety and other aspects of the disease, and provide more optional treatment options for patients, and also provide more exploration paths for the pathogenesis of VKH syndrome.

[0005] Magnesium is a mineral necessary for maintaining life activities, is a more abundant divalent cation in cells, participates in protein synthesis, energy generation and storage and other basic biological processes, and can regulate the functions of the innate and adaptive immune systems. Magnesium Transporter 1 (MAGT1) is a magnesium ion transporter located on the cell membrane, which plays an important role in the glycoprotein N-glycosylation process of platelets. Studies have shown that MAGT1 gene deficiency is related to X-linked immunodeficiency and EB virus infection. At present, there are few studies on MAGT1, and there is no relevant research report on MAGT1 in autoimmune diseases, and the function and mechanism of MAGT1 in patients with VKH syndrome are still unknown. Therefore, the research on MAGT1 gene can provide a new target and an exploratory treatment plan for the treatment of VKH syndrome patients, and is expected to find a new breakthrough for the prevention and treatment of the disease. SUMMARY

[0006] To achieve the above technical purpose, the present application provides an application of MAGT1 small interfering RNA in preparation of a drug for treating uveitis.

[0007] The technical scheme of the present application is as follows: The application of MAGT1 small interfering RNA in preparation of a drug for treating uveitis, wherein the MAGT1 small interfering RNA is RNA for interfering and reducing the expression amount of MAGT1.

[0008] Further, the MAGT1 small interfering RNA is RNA for reducing the expression amount of MAGT1 in CD4 + T cells, thereby inhibiting the proportion of Th1 cells and Th17 cells in CD4 + T cells.

[0009] The MAGT1 small interfering RNA is RNA for reducing the expression amount of MAGT1 in CD4 + T cells, thereby increasing the proportion of Treg cells in CD4 + T cells.

[0010] Still further, the MAGT1 small interfering RNA reduces the expression amount of MAGT1 in CD4 + T cells, reduces the proportion of Th1 cells and Th17 cells in CD4 + T cells, and increases the proportion of Treg cells, thereby inhibiting uveitis.

[0011] Further, the MAGT1 small interfering RNA comprises MAGT1-si1 and MAGT1-si2.

[0012] Further, the nucleotide sequence of the MAGT1-si1 is 5'-GAAAGCCCCACCGAGAAAUTT-3'.

[0013] The nucleotide sequence of the MAGT1-si2 is 5'-GAUGAAGGCUCUGAUGUAUTT-3'.

[0014] Further, the drug for treating uveitis is a drug for treating Vogt-Koyanagi-Harada syndrome.

[0015] Further, the drug for treating uveitis is a drug for treating Vogt-Koyanagi-Harada syndrome by down-regulating the expression of MAGT1.

[0016] Further, the drug for treating uveitis at least comprises an RNA as an active ingredient for interfering or reducing the expression of MAGT1.

[0017] Advantages of the present application: The present application uses ionomics technology and in vitro molecular experiments to find that the expression level of magnesium ion transporter gene MAGT1 in CD4 + T cells of VKH syndrome patients in the active stage is significantly increased, so the MGT1 small interfering RNA provided by the present application can efficiently knock down the expression of MGT1 protein, down-regulate the proportion of Th1 cells and Th17 cells in CD4 + T cells, and up-regulate the proportion of Treg cells, thereby inhibiting uveitis, especially Vogt-Koyanagi-Harada syndrome, which supplements the pathogenesis of uveitis and provides a new strategy for target treatment. BRIEF DESCRIPTION OF DRAWINGS

[0018] Figure 1 FIG. 1 is the ionomics integration analysis results of the serum and CD4 + T cells of the VKH syndrome patients in Example 1; wherein A is the difference analysis wein diagram of the contents of 8 ions in the serum and CD4 + T cells of the VKH syndrome patients and healthy controls, B is the content diagram of magnesium ions in the serum of the VKH syndrome patients and healthy controls, and C is the content diagram of magnesium ions in the CD4 + T cells of the VKH syndrome patients and healthy controls; Figure 2 FIG. 2 is the ionomics integration analysis results of the serum and CD4 +Flow cytometry diagrams illustrating the effects of Th1, Th17, and Treg cell proportions on T cell expression levels. Magnesium ion supplementation used was magnesium L-threonate (MgT), and the negative control (NC) consisted of treatment with an equal volume of double-distilled water. Figure A shows the flow cytometry analysis of Th1 and Th17 cell proportions in the NC and 50 μM MgT groups; Figure B shows the flow cytometry analysis of Treg cell proportions in the NC and 50 μM MgT groups; Figure C shows the differential expression of Th1 cell proportions between the NC and 50 μM MgT groups; Figure D shows the differential expression of Th17 cell proportions between the NC and 50 μM MgT groups; and Figure E shows the differential expression of Treg cell proportions between the NC and 50 μM MgT groups. Figure 3 CD4 in patients with VKH syndrome and healthy controls (HC) in Example 1 + Schematic diagram of MAGT1 expression levels in T cells; Figure 4 To investigate the effect of MAGT1 interference on CD4 in patients with VKH syndrome + Flow cytometry diagram showing the effects of the proportions of Th1 cells, Th17 cells, and Treg cells in T cells on expression levels. Detailed Implementation

[0019] CD4 + T cells are a type of T cell that participate in the immune response. They can differentiate into various types of T helper cells (Th cells).

[0020] Th1 cells secrete a substance called interferon-γ (IFN-γ). + The inflammatory factors, denoted as IFN-γ + CD4 + T cells.

[0021] Th17 cells secrete interleukin-17 (IL-17). + The T cell subset, counted as IL-17 + CD4 + T cells.

[0022] Treg cells secrete Foxp3 + CD25 + Regulatory T cells, counted as Foxp3 + CD25 + CD4 + T cells.

[0023] Example 1: 1. CD4 + T cell isolation and collection (1) Collect peripheral blood of VKH syndrome patients and healthy controls into EDTA-K2 anticoagulant tubes, and immediately invert the blood sample in the tube to prevent blood coagulation; (2) Clean the clean bench, and place the pipette, pipette tip, glass tube, centrifuge tube, and Pasteur tube in the clean bench, and turn on the ultraviolet irradiation for about 30 minutes; (3) Place the collected blood sample in the ultraviolet disinfected clean bench, transfer the blood to a 50ml centrifuge tube, dilute the blood with an equal volume of sterilized PBS, and mix gently; (4) Take about 3ml of human lymphocyte separation medium and add it to a sterilized glass tube, and slowly add the diluted blood sample along the wall of the tube to the upper layer of the lymphocyte separation medium using a disposable Pasteur tube, keeping the boundary clear, and sealing the glass tube with a sterile sealing film; (5) Use gradient centrifugation method, centrifuge at 4℃, centrifugal force 800g, acceleration 4 up and 0 down, for 30 minutes; (6) After centrifugation, carefully remove the glass tube, avoid shaking to affect cell layering, carefully aspirate the cloud-like middle cell layer with a Pasteur tube in the clean bench and move it to a 15ml centrifuge tube, add PBS to the 12ml mark of the centrifuge tube, and gently blow and wash the cells with a Pasteur tube; (7) Centrifuge at 1400rpm for 10 minutes at room temperature; (8) Discard the supernatant in the clean bench, avoid light, and add CD4 magnetic beads and magnetic bead buffer according to the recommended proportion (1x10 7 cells require 20μl of CD4 magnetic beads and 80μl of magnetic bead buffer), mix gently, incubate in a 4℃ refrigerator for 15-20 minutes, and avoid light; (9) Take out the incubated sample, add 2ml of magnetic bead buffer to the incubated cells in the clean bench, mix gently, and centrifuge at 1250rpm for 8 minutes with a low-speed centrifuge; (10) Place the MS sorting column on the Miltenyi MACS magnetic stand, and add 500μl of magnetic bead buffer to wet the sorting column; (11) Take out the centrifuged sample, discard the supernatant, resuspend the cells by adding 1ml of magnetic bead buffer, and add the cell suspension to the column when the magnetic bead buffer in the MS sorting column is dropped; (12) When the cell suspension is almost dropped, rinse the centrifuge tube containing the incubated cells with 500μl of magnetic bead buffer, and add the liquid to the MS sorting column; (13) After all the liquid in the MS sorting column drips out, use tweezers to remove the column and transfer it to a new 15 ml centrifuge tube. Add 1 ml of magnetic bead buffer to the column and use the matching column core to quickly push the liquid into the centrifuge tube. Repeat once; (14) Discard the MS sorting column. Centrifuge the cell suspension collected in the previous step at 1250 rpm for 6 minutes using a low-speed centrifuge. Discard the supernatant. At this time, the sediment in the centrifuge tube is CD4 + T cells; (15) Resuspend the separated CD4 + T cells with 1 ml of PBS. Divide the cell suspension into two 1.5 ml centrifuge tubes. Centrifuge at 4°C, 6000 rpm for 10 minutes using a low-temperature centrifuge. Discard the supernatant. Store the cell sediment at -80°C for future use and ionomics detection.

[0024] 2. Isolation and collection of serum (1) Collect peripheral blood from VKH syndrome patients and healthy controls into a coagulation tube; (2) Pre-cool the centrifuge to 4°C. Centrifuge at 4°C, 2000g for 10 minutes. (3) Take out the centrifuged sample and take the supernatant, which is serum. Store the serum at -80°C for future use and ionomics detection.

[0025] 3. CD4 + T cell ionomics sequencing (1) Sample processing: Each sample is diluted to 5 mL with ultrapure water, ultrasonicated at 100W for 5 minutes, and mixed well before being loaded onto the machine.

[0026] (2) Machine detection: Use inductively coupled plasma mass spectrometry (Thermo X Series II, Thermo Fisher) and inductively coupled plasma emission spectrometry (ICAP6300, Thermo Fisher) to determine the content of 32 elements in the cell sample. The detection parameters are as follows: Table 1 Inductively coupled plasma mass spectrometer

[0027] Table 2 Inductively coupled plasma emission spectrometer

[0028] (3) Qualitative analysis by element-specific mass number (mass-to-charge ratio, m / z). Quantitative analysis is performed by the intensity ratio of the mass spectrum signal of the element to be tested to the mass spectrum signal of the internal standard element, which is proportional to the concentration of the element to be tested.

[0029] (4) Data preprocessing: 27 peaks were extracted from the original data, and single peak filtering was performed to remove noise. No outlier filtering was performed based on the original data. Single peak filtering was performed to retain only ions with no more than 50% missing values in a single group or no more than 50% missing values in all groups. Missing values in the original data were simulated using a numerical simulation method of one-half of the minimum value. After preprocessing, 27 peaks were retained.

[0030] (5) The data was analyzed using multivariate statistical analysis methods, and the p value was calculated using Student's t-test method for statistical analysis. The screening criteria for differential ions were set as ions with p < 0.05.

[0031] 4. Serum ion group sequencing (1) Sample processing: Take 0.1 g of serum sample, treat with 30% hydrogen peroxide overnight, then dilute directly with deionized water to 1.5 g, and centrifuge, take the supernatant for machine; (2) First ignite the plasma, instrument tuning calibration, after passing about 30 min, sample injection, machine detection: Table 3 Inductively coupled plasma mass spectrometer

[0032] (3) Qualitative analysis by element-specific mass number (mass-to-charge ratio, m / z), quantitative analysis by internal standard method, the intensity ratio of the mass spectrum signal of the element to be tested to the mass spectrum signal of the internal standard element is proportional to the concentration of the element to be tested.

[0033] (4) Data preprocessing: 27 peaks were extracted from the original data, and single peak filtering was performed to remove noise. No outlier filtering was performed based on the original data. Single peak filtering was performed to retain only ions with no more than 50% missing values in a single group or no more than 50% missing values in all groups. Missing values in the original data were simulated using a numerical simulation method of one-half of the minimum value. After preprocessing, 27 peaks were retained.

[0034] (5) The data was analyzed using multivariate statistical analysis methods, and the p value was calculated using Student's t-test method for statistical analysis. The screening criteria for differential ions were set as ions with p < 0.05.

[0035] 5, 1.09*10 -7 RNA extraction and detection of cells (1) Set the low-temperature centrifuge to 4°C pre-cooling, and perform RNA extraction in the biological safety cabinet; (2) Take out 1.09*10 -7Cells, add 1 ml Trizol, repeatedly blow the cells to the cells to be fully lysed, room temperature for 5-10 minutes; (3) Add 200 μl of chloroform, cover the centrifuge tube cover, reverse mixing, room temperature for 10 minutes; (4) Use low-temperature centrifuge at 4°C, 12000 rpm, acceleration 9, 9, centrifuge for 15 minutes; (5) After centrifugation, carefully remove the centrifuge tube to avoid shaking, and transfer the uppermost transparent liquid to a new 1.5 ml enzyme-free centrifuge tube; (6) Add 500 μl of isopropyl alcohol, mix the centrifuge tube, and stand at room temperature for 10-20 minutes; (7) Use low-temperature centrifuge at 4°C, 12000 rpm, acceleration 9, 9, centrifuge for 10 minutes; (8) Prepare 75% ethanol solution with anhydrous ethanol and ultrapure water, discard the supernatant after centrifugation, add 1 ml of 75% ethanol solution, and mix gently; (9) Use low-temperature centrifuge at 4°C, 8000 rpm, acceleration 9, 9, centrifuge for 8 minutes, carefully remove the supernatant, and add an appropriate amount of enzyme-free water to dissolve the precipitate when the tube is dry; (10) The RNA solution obtained by extraction is determined by NanoPhotometer spectrophotometer for concentration and purity, and the RNA is stored at -80°C for standby.

[0036] 6. Real-time fluorescent quantitative PCR reaction (RT-qPCR) (1) Reverse transcription: gDNA digestion treatment: prepare the reaction solution of the following components in an enzyme-free 200 μl centrifuge tube on ice, gently mix with a pipette, and incubate at 42°C for 2 minutes after instantaneous separation.

[0037] Table 4 PCR reverse transcription conditions

[0038] (2) Reverse transcription: take the incubated sample in the first step, add 10 μl of gDNA digester inhibitor 2x Super RT Mix (20 μl system) in the centrifuge tube, gently mix with a pipette, and react in the PCR instrument according to the following program after instantaneous separation.

[0039] Table 5 PCR reverse transcription parameters

[0040] (3) The product obtained by the reaction is cDNA, and the synthesized cDNA is stored at -20°C for short-term storage, and stored at -80°C for long-term storage to avoid repeated freezing and thawing of the sample.

[0041] Real-time PCR (1) Prepare the PCR reaction system with the following components on ice: Table 6 PCR reaction system

[0042] (2) Perform real-time fluorescent quantitative PCR reaction using ABI 7500 fluorescent quantitative PCR instrument according to the following procedure.

[0043] 7. Establishment and identification of MAGT1 siRNA interference model (1) Establishment of interference model: collect peripheral blood from 6 patients with active VKH syndrome, separate CD4 + T cells by Ficoll-Hypaque density gradient centrifugation, and randomly divide the cells into 3 treatment groups, siNC group and MAGT1-si1 and MAGT1-si2 groups. siNC is the negative control group; MAGT1-si1 sequence is: 5'-GAAAGCCCCACCGAGAAAUTT-3', and MAGT1-si2 sequence is: 5'-GAUGAAGGCUCUGAUGUAUTT-3'; sequence design and product purchase from Shanghai Biotechnology. Then, according to the adenovirus and lip3000 plasmid transfection instructions, perform PARP10 interference treatment, and perform in vitro culture, add CD3 / 28 to stimulate CD4 + T cell activation, collect cell precipitate after 3 days of culture of treated cells.

[0044] (2) Identification: identification by RT-qPCR method, as described above. Identification by Western blot method. Western blot detection: add 100 μl RIPA protein lysis buffer and protease inhibitor to each culture dish, and store at -80°C for lysis. The next day, after centrifugation of the sample at 12000 rpm at 4°C for 15 min, collect the supernatant, i.e. protein lysis buffer, determine the protein concentration by BCA method, and perform Western blot protein immunoblotting analysis.

[0045] 8. Statistical analysis ​Statistical analysis was performed using GraphPad Prism V.7.0.0. Shapiro-Wilk normality test was used to test whether the data belonged to normal distribution, for normally distributed data, independent sample t test and one-way ANOVA were used to test the variance analysis between groups, and the statistical results were shown as Mean ± SD; for data not belonging to normal distribution, Mann-Whitney test and Kruskal-Wallis test were used for variance analysis between groups, and the statistical results were shown as Median. All statistical results were taken as the criterion for statistical significant difference of p < 0.05.

[0046] 9. Experimental results and analysis conclusion (1) MAGT1 is a key gene in the pathogenesis of VKH syndrome ① We used ionomics technology to detect the serum of 20 cases of active period without drug VKH syndrome patients and 20 cases of healthy controls, and set p value < 0.05 as the screening standard of differential ions, found that the content of 8 kinds of ions in the serum of VKH syndrome patients was significantly reduced, and the content of 1 kind of ion was significantly increased. In addition, we used ionomics technology to detect the CD4 + T cells in the peripheral blood of 6 cases of active period without drug VKH syndrome patients and 6 cases of healthy controls, and set p value < 0.05 as the screening standard of differential ions, found that the content of 5 kinds of ions in CD4 + T cells of VKH syndrome patients was significantly reduced.

[0047] ② Through integrated analysis of the ionomics results of serum and CD4 + T cells of VKH syndrome patients, we found that the content of magnesium ions in the serum and CD4 + T cells of VKH syndrome patients was significantly reduced, see Figure 1 .

[0048] ③ According to the ionomics sequencing results, we found that the VKH syndrome patients were magnesium deficient, so we set up a magnesium supplement experiment. Specifically, we isolated and extracted the CD4 + T cells of the above-mentioned VKH syndrome patients without drug, cultured them in vitro and added CD3 / 28 to stimulate cell activation, and at the same time, we treated the cells with 50 μM concentration of L-threonic acid magnesium (i.e. magnesium supplement treatment group, counted as 50 μM MgT group), and collected the cells for detection after 2 days of culture), we detected the effect of 50 μM magnesium ion supplement on CD4 +The influence on the balance of Th1, Th17 / Treg cells in CD4+T cells. From the flow cytometry results, we can see that compared with the negative control group (NC group), the proportion of Th1 and Th17 cells in the 50 μΜ MgT group was significantly reduced, while the proportion of Treg cells was significantly increased, see Figure 2 .

[0049] ③Then, we detected the expression of CD4 + T cells in 9 VKH syndrome patients and 9 healthy controls. We detected the expression of 5 common magnesium ion transporter genes (MAGT1, SLC41A1, TRPM7, NIPA1 and NIPA2) in CD4 + T cells by RT-qPCR. The results showed that only MAGT1 was differentially expressed when the p-value was set to be less than 0.5. The expression of MAGT1 in CD4 Figure 3 .

[0050] (2) The proportion of Th1 and Th17 cells in CD4 + T cells was reduced, and the proportion of Treg cells was increased after MAGT1 interference.

[0051] We isolated and extracted CD4+T cells from 3 VKH syndrome patients in active stage without medication, and found that compared with the siNC group, the proportion of Th1 and Th17 cells in the CD4 + T cells of the MAGT1-si1 and MAGT1-si2 groups was significantly reduced, and the proportion of Treg cells was significantly increased, i.e. inhibiting the expression of MAGT1 can reduce the proportion of Th1 and Th17 cells in CD4 + T cells, and increase the proportion of Treg cells, see Figure 4 . The above research results suggest that MAGT1 is a potential pathogenic molecule of VKH syndrome, which may induce the occurrence of the disease by regulating the balance of Th1, Th17 / Treg cells in CD4 + T cells.

Claims

1. Use of MAGT1 small interfering RNA in the preparation of a medicament for treating uveitis, characterized in that, The MAGT1 small interfering RNA is RNA interfering with or reducing the expression of MAGT1.

2. Use of the MAGTl small interfering RNA according to claim 1 for the preparation of a medicament for the treatment of uveitis, characterized in that, The MAGT1 small interfering RNA is by down-regulating CD4 + MAGT1 expression in T cells, thereby inhibiting CD4 + RNA of the ratio of Th1 cells and Th17 cells in T cells.

3. Use of the MAGTl small interfering RNA according to claim 1 for the preparation of a medicament for the treatment of uveitis, characterized in that, The MAGT1 small interfering RNA is by down-regulating CD4 + MAGT1 expression in T cells thereby increasing CD4 + Treg cell proportion in T cells.

4. Use of the MAGTl small interfering RNA according to claim 1 for the preparation of a medicament for the treatment of uveitis, characterized in that, The MAGT1 small interfering RNA inhibits uveitis by down-regulating CD4 + MAGT1 expression in T cells, decreasing CD4 + The ratio of Thl cells and Thl7 cells in T cells, increasing the ratio of Treg cells, thereby inhibiting uveitis.

5. Use of a MAGTl small interfering RNA according to any one of claims 1 to 4 for the preparation of a medicament for the treatment of uveitis, characterized in that, The MAGT1 small interfering RNA includes any one or more of MAGT1-si1 and MAGT1-si2.

6. Use of the MAGTl small interfering RNA according to claim 5 for the preparation of a medicament for the treatment of uveitis, characterized in that, The nucleotide sequence of the MAGT1-si1 is 5'-GAAAGCCCCACCGAGAAAUTT-3'.

7. Use of the MAGTl small interfering RNA according to claim 5 for the preparation of a medicament for the treatment of uveitis, characterized in that, The nucleotide sequence of the MAGT1-si2 is 5'-GAUGAAGGCUCUGAUGUAUTT-3'.

8. Use of a MAGTl small interfering RNA according to any one of claims 1 to 5 for the preparation of a medicament for the treatment of uveitis. The drug for treating uveitis is a drug for treating Vogt-Koyanagi-Harada syndrome.

9. Use of the MAGTl small interfering RNA according to claim 8 for the preparation of a medicament for the treatment of uveitis, characterized in that, The drug for treating uveitis is a drug for treating Vogt-Koyanagi-Harada syndrome by down-regulating the expression of MAGT1.

10. Use of the MAGTl small interfering RNA according to claim 1 for the preparation of a medicament for the treatment of uveitis, characterized in that, The drug for treating uveitis at least includes RNA interfering with or reducing the expression of MAGT1 as an active ingredient.

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