Modulation of HLA antigen expression on conjunctival fibroblasts by gamma-interferon

We investigated the ability of recombinant human gamma-interferon (rhIFN-gamma) to induce class II HLA antigen expression on human conjunctival fibroblasts in cell culture. Cultures were established by explanting subconjunctival tissue from normal donor globes. Fibroblasts were treated with rhIFN-gamma at concentrations ranging from 1 to 500 units/ml and incubated for 1, 3 and 6 days. HLA antigens were detected by immunofluorescence using monoclonal antibodies in conjunction with flow cytometry. Class I antigen was identified using a monoclonal antibody directed against Beta-2 microglobulin (a component of the class I antigen complex). Class II histocompatibility antigens were detected using monoclonal antibodies specific for HLA-DR, HLA-DP and HLA-DQ. Class I antigen was present on all cells prior to induction and showed a trend toward increased density after treatment with rhIFN-gamma. Class II antigens were absent before induction with rhIFN-gamma. After treatment with rhIFN-gamma, class II antigens were induced in a dose- and time-dependent fashion. HLA-DR expression was most sensitive to induction by rhIFN-gamma, followed by HLA-DP, and then HLA-DQ. The up-regulation of HLA class I antigen expression and the inducible expression of class II antigens following exposure to rhIFN-gamma suggest that conjunctival fibroblasts have the potential to participate in immunologic diseases of the external eye.     

Regulation of HLA class II antigen expression on cultured corneal epithelium by interferon-gamma.

The effect of recombinant human interferon gamma (IFN-gamma) on the induction of HLA class II (HLA-DR, -DP, -DQ) antigen expression on human corneal epithelial (HCE) cells was examined in different stages of culture. Primary cultures were established with limbal explants without endothelium. HCE cells in Stage 1 and Stage 2, with cells negative and positive for the 64K corneal keratin (the marker for advanced corneal epithelial differentiation), respectively, were prepared. HCE cells in both stages were treated with IFN-gamma at a concentration of 0 to 1000 U/ml for two to six days and were stained by the avidin-biotin peroxidase complex method. Class II antigens were not detected on HCE cells in either stage without IFN-gamma treatment. IFN-gamma induced three class II antigens on HCE cells in both stages in a dose- and time-dependent manner but at different levels for each antigen (DR greater than DP greater than DQ). In addition, DQ expression was related to cell differentiation, with DQ extremely rare at Stage 1 and more frequent at Stage 2 (5% vs. 20%). These findings indicate that the induction of class II antigens on HCE cells may be regulated by IFN-gamma independently for each of the antigens and that DQ induction may depend upon the differentiation of HCE cells in culture.     

Detection of HLA antigens in human epikeratophakia lenticules

We compared the distribution of HLA-ABC (Class I) and HLA-DR, -DQ, and -DP (Class II) antigens in fresh, non-lyophilized human cornea with that of rehydrated lyophilized epikeratoplasty lenticules. Class I antigens were detected at similar levels in both the control corneas and the epikeratophakia lenticules. Class II antigens, which were limited to cells at the limbus of control corneas, were absent from the epikeratophakia lenticules. Although epikeratophakia lenticules are not necessarily immunogenic, these results clearly demonstrate that they are antigenic and express selected major histocompatibility antigens. In the context of these findings, we discuss the lack of reports of immunologic rejection following epikeratoplasty.     

Gamma-interferon induces differential expression of HLA-DR, -DP and -DQ in human ciliary epithelial cells

The antigen-specific activation of T-helper lymphocytes is dependent on the presentation of antigen in context with the gene products of the major histocompatibility complex class II (MHC 1I). Aberrant expression of MHC 11 on the ciliary epithelium has been observed in uveitic eyes which may enable these cells to specifically interact with lymphocytes and may play a role in ocular autoimmunity. Human MHC II consists of three subclasses termed HLA-DR, -DP and -DQ, which seem to be differentially regulated and may have different functions. The present study was initiated to investigate the dynamics of the differential MHC II expression on cultured human non-pigmented ciliary epithelial cells (NPE cells) in response to gamma-interferon (gamma-IFN) by means of immunohistochemistry. NPE cells grown in control tissue-culture medium did not express MHC class II. HLA-DR and -DP could be induced by incubation with 100 u/ml gamma-IFN for 3 days. HLA-DQ was expressed only weakly and at higher doses of gamma-IFN ( 500 a/ml) and longer incubation periods ( 5 days). After removal of the gamma-IFN stimulus, all three MHC II subclasses persisted for several days. The differential expression of HLA-DR and -DP as compared with HLA-DQ in response to gamma-IFN in the ciliary epithelium is similar to observations in other non-lymphoid ocular cells but appears to be different from the regulation of MHC II expression on lymphoid cells. Since HLA-DR and -DP seem to be linked mainly to immune-response genes, whereas a linkage to immune suppressor genes has been described for HLADQ, the MHC II expression on bone marrow-derived cells and non-lympoid ocular cells may serve different functions.H.H. is the recipient of a scholarship of the Deutsche Forschungsgemeinschaft     

Immunohistologic study of epiretinal membranes in proliferative vitreoretinopathy.

We performed an immunohistologic study on 11 specimens of epiretinal membranes surgically obtained from patients who had rhegmatogenous retinal detachment with proliferative vitreoretinopathy. Immunostaining procedures were used to identify immunoglobulin and complement deposits, to visualize class II antigen expression by proliferating cells, and to determine eventual infiltration by cells of the immune system. Diffuse deposits of IgG, IgA, IgE, C1q, C3c, and C3d were found in epiretinal membranes, whereas numerous cells, including glial or pigmented epithelial cells, expressed HLA-DR and HLA-DQ antigens. Some macrophages and B or T8 lymphocytes were identified. These results suggest activation of the immune system during the course of proliferative vitreoretinopathy. Class II antigen expression could be dependent upon growth-promoting factors and interferon gamma and could play a crucial role in this immune reaction, which resulted in immunoglobulin deposition and activation of complement. However, the eventual role of immune phenomena in the extension of proliferative processes remains to be determined.     

HLA-antigens in the human uvea

With the use of monoclonal antibodies in an indirect immunofluorescence technique we studied the distribution of Class I (HLA-ABC and B27) and Class II (HLA-DR) antigens in the human uvea. W6/32, directed against the core of HLA-ABC antigens, was used to study the distribution of Class I antigens. The anterior border layer of the iris, the non-pigmented and pigmented epithelium and the external basement membrane of the ciliary body and the vascular endothelium in the uvea showed a positive staining for Class I antigens. B27/M1, directed against an epitope of the HLA-B27 antigen, and the control antibody A11/Aw24, which was directed against an epitope of HLA-A11, revealed the same distribution pattern in respectively HLA-B27 and HLA-A11 positive donor eyes. The intensity of their staining was much weaker than the staining with W6/32.Class II antigens were studied with OkIal, an antibody directed against the core of HLA-DR antigens. HLA-DR antigens were detectable on single cells scattered throughout the entire uvea. These cells did not seem to relate to any anatomical entity. No staining for Class II antigens was seen in the uveal blood vessel endothelium.The expression of HLA-antigens in the uvea is compatible with the distribution in other tissues. These findings suggest that the expression of HLA-B27 in the human uvea does not explain why the eye is one of the target tissues in HLA-B27 associated disease.     

Class II induction of human corneal fibroblasts by cell-free supernatants from HSV stimulated lymphocytes

Lymphocytes obtained from patients with herpes simplex virus, type 1 (HSV) neutralizing antibodies were stimulated in vitro for 48 hr with heat inactivated HSV. Cell-free supernatant from these cultures was added to autologous or allogeneic HLA-DR-negative stromal (fibroblast) cells for 3 days. All stromal cultures were stained with monoclonal reagents by indirect immunofluorescence for Class I (beta 2) or Class II (HLA-DR) antigen expression. Supernatant from HSV-stimulated lymphocytes induced HLA-DR antigen on cultured stromal cells while supernatant from lymphocytes cultured in the absence of HSV antigen or from lymphocytes which did not proliferate in response to incubation with HSV antigen did not induce HLA-DR. The expression of Class II antigens induced by supernatant from HSV-stimulated lymphocytes was inhibited by the addition of purified antibodies to IFN.     

Modulation of HLA antigen expression on corneal epithelial and stromal cells

Human corneal epithelial cells and stromal fibroblasts in culture were incubated with gamma interferon or with medium conditioned by phytohemagglutinin (PHA)-stimulated mononuclear cells. The corneal cells were placed into suspension, assayed for class I (HLA-A,B,C) and class II (HLA-DR) antigens by indirect immunofluorescence, and analyzed with flow cytometry. Epithelial cells treated for 5 days with conditioned medium (CND-M) did not exhibit an increase in class I or an induction of class II antigen expression, although a trend toward increased class I antigen expression was present. Epithelial cells treated for 5 days with 250-500 U/ml of gamma interferon did not demonstrate an increase in class I but did show an induction of class II antigen expression; again, however, a trend toward increased class I antigen expression was present. Stromal fibroblasts treated for 3-5 days with CND-M exhibited an increase in class I antigen expression, but stromal fibroblasts treated for 1-5 days with CND-M did not show an induction of class II antigen expression. Stromal fibroblasts incubated for 1-5 days with 250-750 U/ml of gamma interferon demonstrated both an increase in class I and an induction of class II antigen expression. These data suggest that host lymphokines may intensify the process of corneal graft rejection by augmenting class I antigen expression on allogeneic cells. Moreover, the induction of class II antigen expression by host lymphokines on cells in transplanted corneal tissue may lead to host sensitization and subsequent allograft rejection.     

HLA antigenicity of normal and pathological corneas

Fresh human corneas and corneal buttons were studied for expression of HLA antigens. Using monoclonal antibodies in an indirect immunofluorescence assay, corneal layers were examined for class I (HLA-A, B, C) and class II (HLA-DR) histocompatibility antigens. Twenty-one human corneas were studied, 6 normal and 15 pathological: 4 buttons of allograft rejection, 9 buttons of pseudophakic bullous keratopathy. In fresh control corneas, HLA-A, B, C antigens were localized on corneal epithelium and on stromal keratocytes but were never found on endothelial cells. HLA-DR antigens were not detected on corneal epithelium, stroma or endothelium but were detected on Langerhans cells within epithelium and anterior stroma. At the corneal limbus, HLA class I-II antigens were expressed on vascular endothelium. HLA antigen distribution was modified in pathological corneas. Antigens HLA-A, B, C were induced on endothelial cells of rejected corneal allografts. Antigens HLA-DR were detected on epithelial cells, cells in the stroma of pseudophakic bullous keratopathy and also on endothelial cells of rejected corneal allografts. These results suggest that induction of class I and II antigen expression by inflammatory factors may occur in vivo. In rejected corneal allografts induction of HLA-DR antigen on corneal layers would intensify the process of rejection. This study and others have demonstrated the ability of modulation of HLA antigen expression on human corneal cells in vivo.     

人视网膜色素上皮细胞与T淋巴细胞的激活

目的 观察人视网膜色素上皮（RPE）细胞人类白细胞抗原(HLA)-DP、-DQ、-DR抗原和CD40抗原的表达，以确定它们在免疫应答过程中的分子表达和刺激T淋巴细胞活化的能力。方法 人RPE细胞分别在γ-干扰素诱导和无诱导的条件下培养，免疫组织化学染色方法测定HLA-DP、-DQ、-DR抗原和CD40抗原在RPE细胞中的表达。体外共同培养人RPE细胞和外周血单个核细胞，荧光活化细胞分类仪测定其中活化的T淋巴细胞CD69的表达。结果 γ-干扰素能够诱导HLA-DP、-DQ、-DR抗原表达升高和CD40在人RPE细胞上的表达，CD69阳性的T淋巴细胞，在人RPE细胞与外周血单个核细胞的共同培养系统中的含量增加。结论 人RPE细胞能够激活外周血中T淋巴细胞，是一种具有免疫学特性潜能的抗原递呈细胞。     

HLA-A,B,C, and HLA-DR antigens and dendritic cells in fresh and organ culture preserved corneas

Fresh and organ-culture preserved human corneas were examined for HLA-A,B,C (class I) and HLA-DR (class II) histocompatibility antigens using mouse monoclonal antibodies and an indirect immunofluorescence technique. HLA-A,B,C antigens were detected on epithelial cells and on keratocytes, but not on endothelial cells in fresh corneas. The expression of HLA-A,B,C antigens was not significantly altered by organ-culture for a period up to 7 days. The epithelial cell layer bearing the larger part of the HLA-A,B,C antigens decreased, however, from 6-7 layers to 2-3 during organ culture. HLA-DR antigens were not detected on any of the corneal layers, but were present on scattered dendritic cells within the corneal epithelium and on cells in the corneal stroma just beneath the Bowman's membrane. Using immunofluorescence, no cells bearing HLA-DR antigens were seen in cornea sections obtained after 1 week in organ-culture. These results demonstrate that the presence of HLA antigens, particularly of the HLA-DR antigens, is affected by the organ-culture preservation of the human cornea.     

Association of HLA with Vogt-Koyanagi-Harada syndrome in Koreans

PURPOSE: To study the distribution of human leukocyte antigen HLA-A/B antigens and HLA-DR/-DQ/-DP alleles and to investigate the immunogenetic background of Korean patients with Vogt-Koyanagi-Harada (VKH) syndrome and clinical course with different types of HLA. METHODS: Human leukocyte antigen typings were performed in 18 Korean patients with VKH syndrome and in 128 healthy control subjects. HLA-A/B loci serologic typing was performed according to the standard microlymphocytotoxicity technique. DNA was extracted through the salting out method, and HLA-DR phenotyping and HLA-DR4, HLA-DQ, and HLA-DP subtyping were performed with the polymerase chain reaction-sequence specific oligonucleotide probe (PCR-SSOP) method. RESULTS: Among HLA-A/B antigens typed by the standard microlymphocytotoxicity method, the frequencies of HLA-A31 (RR = 6.1, P<1x10(-2)) and HLA-B55 (RR = 15.8, P<.05) were significantly increased in the patient group compared with the control group. Among HLA-DR/-DQ/-DP alleles subtyped by DNA methods, the frequencies of HLA-DRB1*04 (RR = 45.1, P<1x10(-7)) and HLA-DRB1*07 (RR = 3.2, P<.05) were significantly increased. However, significant decreases in HLA-DRB1*08 (RR = .1, P<.05), HLA-DRB1*13 (RR = .1, P<.05), and HLA-DRB1*14 (RR = .1, P<.05) frequencies were observed. The result of HLA-DR, HLA-DQ, and HLA-DP subtyping showed the significant increase in DRB1*0405 (RR = 45.1, P<1x10(-7)), DQA1*0302 (RR = 12.0, P<1x10(-4)), DQB1*0303 (RR = 5.0, P<1x10(-2)), DQB1*0401 (RR = 18.9, P<1x 10-6), and DPB1*0501 (RR = 3.8, P<.05). However, significant decreases in DQA1*0101 (RR = .1, P< .05), DQA10102 (RR = .1, P<1x10(-2)), DQA1*0103 (RR = .1, P<.05), DQA1*0501 (RR = .1, P<1x10(-2)), DQB1*0301 (RR = .1, P<.05), DQB1*0601 (RR = .1, P<.05), DPB1*0201 (RR = .3, P<.05), and DPB1*0401 (RR = .1, P<.05) frequencies were also observed. In patients with DRB1*0405 itself or HLA-DRB1*0405-DQA1*0302-DQB1*0401 haplotype, a reduction in visual acuity and ocular complications was common. CONCLUSIONS: These results suggest that HLA-DRB1*0405 itself or HLA-DRB1*0405-DQA1*0302-DQB1*0401 haplotype is greatly increased and may play the most important role in the development and the clinical course of VKH syndrome in Korean patients.     

Effect of human corneal fibroblasts on lymphocyte proliferation in vitro

Cocultivation of human corneal fibroblasts (CFB) with allogeneic peripheral blood mononuclear cells (PBL) induced a minimal lymphocyte proliferative response, even when the fibroblasts had been pre-treated with interferon-gamma (IFN-gamma) and were HLA-DR positive. IFN-gamma-treated CFB did not express detectable HLA-DQ alloantigens. Cocultivation of CFB with PBL in the presence of Concanavalin A (Con A) or Phytohemagglutinin inhibited mitogen-induced lymphocyte proliferation by 40-90% relative to PBL cultured without CFB. Induction of HLA-DR expression on the CFB did not alter their inhibitory properties. Addition of indomethacin to cultures reversed the effect of CFB on Con A responses. However, no difference between proliferative responses to HLA-DR positive or negative CFB was seen in the presence of indomethacin. This weak response to induced Class II alloantigens on CFB suggests that induction of Class II alloantigens on corneal stroma alone may be insufficient to sensitize a recipient for Class II alloantigen-driven corneal graft rejection.     

Expression of HLA class I and II antigens on cells of the human trabecular meshwork

Human corneoscleral tissue containing trabecular meshwork and cultured human trabecular cells were examined for HLA-ABC (class I) and HLA-DR (class II) antigens of the major histocompatibility complex using an indirect immunofluorescence assay. Class I antigens were detected in the trabecular meshwork on frozen sections and on cultured trabecular cells. Class II antigens were constitutively expressed on some, but not all, cells within the trabecular meshwork. Many more cells could be induced to express class II antigens by pre-incubation in human gamma interferon. Cultured trabecular cells did not express class II antigens constitutively, but expression could be induced by gamma interferon. This study suggests that, in addition to Langerhans' cells at the limbus, other cell types within the anterior segment express major histocompatibility complex-encoded class II antigens either constitutively or inducibly. These cells may be important for the initiation and regulation of ocular immunity.     

Immunology of corneal allograft rejection: HLA-DR antigens on human corneal cells

Human stromal and endothelial cultures were established from corneas obtained from the Maryland Eye Bank. Cultures were incubated in the presence of human gamma interferon for 4 days, trypsinized, washed, and then stained with a monoclonal reagent specific for human Class II (HLA-DR) antigens. Under these conditions, 100% of human corneal endothelial cells and 40 to 70% human corneal stromal cells expressed HLA-DR antigens.     

Expression of Ia antigen on retinal pigment epithelium in experimental autoimmune uveoretinitis

Recently, human retinal pigment epithelial (RPE) cells have been demonstrated to express class II, HLA-DR, antigens both in vivo and in vitro. HLA-DR antigens were detected on RPE cells from patients with uveitis and retinitis pigmentosa. In addition, in vitro studies revealed that not only does this cell express HLA-DR antigen but also that this antigen can be modulated by the lymphokine, interferon (IFN)-gamma. In this study we evaluated the development of the murine class II, Ia, antigens on RPE cells in experimental autoimmune uveoretinitis (EAU). Ia antigen was evaluated with the avidin-biotin-peroxidase technique. Ia antigen was not detected on RPE cells from normal rats. However, Ia antigen was detected on the surface of RPE cells from EAU rats four days prior to the development of clinical and histopathological EAU. Moreover, the expression of Ia antigen on RPE cells from EAU rats continued to persist until one and one-half months after immunization. This study demonstrates that during the course of EAU the RPE cell is activated to express Ia antigens. This antigen expression may be important in the initiation and/or perpetuation of immune reactivity in the eye.     

Class II histocompatibility antigen expression by cellular components of vitreous and subretinal fluid in proliferative vitreoretinopathy

Proliferative vitreoretinopathy (PVR) is the major cause of failure in retinal detachment surgery. It is characterized by the formation of membranes extending along both surfaces of the detached retina and within the vitreous, but the nature of the growing cells has not yet been determined. Using cytologic and immunocytologic procedures with 13 different monoclonal antibodies directed against Class II histocompatibility antigens and various markers of epithelial and immunocompetent cells, 30 specimens were studied of vitreous or subretinal fluid removed from patients with PVR. Five main types of cells could be identified: heavily pigmented cells, poorly pigmented ones, large totally unpigmented macrophage-resembling ones, smaller unpigmented cells, and lymphocytes. Analysis of intravitreal pigment granules, using autofluorescence by epiillumination and cytologic procedures, showed two different populations of pigmented cells: one with autofluorescent lipofuscin granules and the other with exclusively melanin pigment. Immunostaining procedures confirmed the epithelial nonmacrophage lineage of the intravitreal and subretinal cells because most of these cells were positive for cytokeratin but negative for macrophage markers. In addition, 40-100% of these epithelial-derived cells strongly expressed Class II histocompatibility antigens HLA-DR and -DQ. Lymphocytes were found in 13 specimens; B-cells were seen, but no T-lymphocytes could be identified. These results confirm the involvement of retinal pigment epithelial cells and the strong morphologic changes they undergo during the course of PVR. Moreover, the expression of Class II histocompatibility antigens by the growing cells may be related to inflammatory phenomena, but their eventual role in the development and the extension of periretinal proliferation has not been determined.     

Vogt-Koyanagi-Harada syndrome in patients of Vietnamese ancestry

Background: Vogt-Koyanagi-Harada syndrome (VKH), is an idiopathic, multisystem inflammatory disorder primarily involving the eye. HLA typing has shown a strong association between the HLA-DR4 antigen and people of Japanese, Han Chinese and Hispanic ancestry with VKH. This study reviewed the clinical features and HLA typing of Vietnamese patients with VKH.
Patients and methods: A retrospective review of four unrelated Vietnamese patients with VKH seen in private practice and hospital clinic. The American Uveitis Society (1978) criteria for VKH diagnosis were satisfied. Standard microcytotoxic assays for Class I antigens and HLA-DNA typing of Class II DR antigens (DRB1 genotyping) by the PCR-SSO method were performed.
Results: The clinical features of VKH in Vietnamese were comparable to those seen in other Asian races. HLA-DR4 was present in three of the four VKH patients. Two of these patients also expressed the allele DRB1*0405.
Discussion: The strong association betlNeen HLA-DR4 and the DRB1*0405 allele and VKH seen in Japanese people, may well also exist in Vietnamese people. The HLA association suggests an immunogenetic predisposition to VKH.     

Stromelysin (matrix metalloproteinase-3) and tissue inhibitor of metalloproteinase (TIMP-1) mRNA expression in scleritis

Scleritis is a severe and destructive inflammatory eye disease characterized by extensive extracellular matrix degradation. As in rheumatoid arthritis (RA), tissue destruction in scleritis may be mediated in part by matrix metalloproteinases such as collagenase (MMP-1) and stromelysin (MMP-3) which are normally kept in balance by endogenous inhibitors, such as tissue inhibitor of metalloproteinase (TIMP-1). To test this hypothesis, in situ hybridization was used to localize MMP-1, MMP-3 and TIMP-1 mRNA in diseased and normal scleral tissue using digoxigenin labelled probes. Strong expression of MMP-3 and TIMP-1 mRNA, but not MMP-1, was observed in the diseased scleral tissue. Infiltrating inflammatory cells such as macrophages and scleral fibroblasts were the primary source of MMP-3 and TIMP-1 expression. There was also relatively less TIMP-1 compared with MMP-3 mRNA expression in the inflammatory cells in scleritis tissue. In order to study regulation of metalloproteinase expression in ocular cells the authors established human scleral fibroblasts (HSF) in primary culture. Northern blot analysis was performed on total RNA extracted from HSF grown in serum free media. MMP-1 MMP-3 and TIMP-1 were constitutively expressed in these cells. Stimulation of HSF with pro-inflammatory cytokines likely to be present in scleritis, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), significantly induced MMP-3 and TIMP-1 mRNA expression. Using culture supernatants derived from the same cytokine stimulated scleral fibroblast the authors were able to detect MMP-3 protein production by Western blot analysis. They conclude that matrix metalloproteinase-3 mRNAs are present in scleritis tissue and may be induced by cytokines produced in the inflammatory process.     

人类永生化角膜内皮细胞的生物学特性

目的探讨人类永生化角膜内皮细胞在免疫反应中的分子表达及其刺激T淋巴细胞活化的能力。方法人类永生化角膜内皮细胞分别培养在含干扰素-γ（IFN-γ）（1000U／mL）和不包含IFN-γ（1000U／mL）的F99和M199培养液中,按照1：1等比例混合并含有5％小牛血清。健康志愿者采集外周血并分离外周血单核细胞（PBMCs）,应用锥虫蓝染色鉴定细胞的完整性和细胞数量。免疫组织化学染色法测定人类永生化角膜内皮细胞分别在有无IFN-γ诱导条件下的HLA—DP、DQ、DR抗原及CD40的表达。同时,体外共同培养人类永生化角膜内皮细胞和PBMCs,荧光活化细胞分类（FACS）法测定活化的T淋巴细胞中CD69的表达。结果IFN-γ能够诱导HLA—DP、DQ、DR抗原和CD40在人类永生化角膜内皮细胞上的阳性表达,表现为细胞膜和细胞质中的红色染色。CD3和CD28抗体预处理的外周血单核细胞中,20％的CD69阳性T淋巴细胞活化,无IFN-γ诱导时有10％阳性T淋巴细胞,而IFN-γ诱导组中,有12％的阳性T淋巴细胞,说明共同培养人类永生化角膜内皮细胞和PBMCs体系中,CD69阳性淋巴细胞数量增加。结论外周血中的T淋巴细胞可以被人类永生化角膜内皮细胞活化,由此人类永生化角膜内皮细胞是具有免疫学特性潜能的抗原递呈细胞。