Biomedical subjects

J Sakai

Publications and source records attributed to J Sakai.

At least 55 records · Page 3Linked to original sources

PubMed1999

Intrauterine growth retardation as a cause of perinatal mortality in Japanese black beef calves.

Perinatal death is one of the major causes of calf mortality in Japanese Black beef herds. A series of experiments were carried out to determine causes of perinatal calf mortality in a region of northern Japan. An aetiological survey revealed that the incidence of perinatal mortality in 6475 calves was 4.5% and the majority of neonatal deaths were caused by weak calf syndrome. The weak calves delivered after a normal gestation period had a significantly lower body weight at birth than normal calves (P < 0.01), indicating growth retardation in the uterus during pregnancy. Haematological and histopathological examinations showed that the weak calves had anaemia characterized by a significant decrease of blood cell values and bone marrow hypofunction. The anaemia due to bone marrow hypofunction presumably caused intrauterine growth retardation of the foetus. Dams delivering the weak calves showed significantly lower serum concentrations of estrone sulphate during late pregnancy than those with normal calves (P < 0.01), indicating foeto-placental dysfunction as a possible cause of growth retardation. Effects of sires as well as the maternal family on the incidence of neonatal death and on the rate of weak calves in dead neonates were found in the survey. Intrauterine growth retardation associated with anaemia may be the most important cause of weak calf syndrome in Japanese Black beef calves. The bull and maternal family may also have an influence on the incidence of neonatal death.

Anemia↗

PubMed1999

Causes of nitrous oxide contamination in operating rooms.

BACKGROUND: To reduce the ambient concentration of waste anesthetic agents, exhaust gas scavenging systems are standard in almost all operating rooms. The incidence of contamination and the factors that may increase the concentrations of ambient anesthetic gases have not been evaluated fully during routine circumstances, however. METHODS: Concentrations of nitrous oxide (N2O) in ambient air were monitored automatically in 10 operating rooms in Kagoshima University Hospital from January to March 1997. Ambient air was sampled automatically from each operating room, and the concentrations of N2O were analyzed every 22 min by an infrared spectrophotometer. The output of the N2O analyzer was integrated electronically regarding time, and data were displayed on a monitor in the administrative office for anesthesia supervisors. A concentration of N2O > 50 parts per million was regarded as abnormally high and was displayed with an alarm signal. The cause of the high concentration of N2O was then sought. RESULTS: During the 3-month investigation, N2O was used in 402 cases. Abnormally high concentrations of N2O were detected at some time during 104 (25.9%) of those cases. The causes were mask ventilation (42 cases, 40.4% of detected cases), unconnected scavenging systems (20 cases, 19.2%), leak around uncuffed pediatric endotracheal tube (13 cases, 12.5%), equipment leakage (12 cases, 11.5%), and others (17 cases, 16.4%). CONCLUSIONS: N2O contamination was common during routine circumstances in our operating rooms. An unconnected scavenging system led to the highest concentrations of N2O recorded. Proper use of scavenging systems is necessary if contamination by anesthetic gas is to be limited.

Air Pollutants, Occupational↗

PubMed1999

Expression of pancreatitis-associated protein (PAP) in rat spontaneous chronic pancreatitis: effect of herbal medicine Saiko-keishi-to (TJ-10).

Pancreatitis-associated protein (PAP) is almost absent in the normal pancreas but is overexpressed in acute pancreatitis. However, its expression in chronic pancreatitis (CP) is unknown. An herbal medicine Saiko-keishi-to (TJ-10) has long been used clinically for CP, but there is no experimental evidence of the effect of TJ-10 on CP. The aim of this study was to analyze the expression of PAP and the effect of TJ-10 in a spontaneous chronic pancreatitis model. Four-week-old male WBN/Kob rats were fed with a special pellet diet (MB-3), and TJ-10 (80 mg/100 g body weight/day) was orally administered for 16 weeks. The rats were killed at every 4 weeks, and pancreata were histopathologically examined. PAP messenger RNA (mRNA) in the pancreas was detected with a reverse transcription/polymerase chain reaction (RT-PCR) method. The cellular localization of PAP mRNA and protein was analyzed with in situ hybridization (ISH) and immunohistochemistry (IHC). PAP mRNA was expressed from 8 weeks, when the pancreas was still pathologically normal, and reached its peak at 12 weeks, when the pancreatitis first appeared. Then the expression of PAP mRNA was decreased gradually. TJ-10 suppressed the expression of PAP mRNA completely at 8 and 12 weeks. PAP mRNA was slightly expressed at 16 and 20 weeks. ISH and IHC confirmed the PAP mRNA and protein expression in the cytoplasm of acinar cells. These results suggest that PAP mRNA appears before CP, and its peak coincides with the onset of CP. TJ-10 suppressed the PAP expression and delayed the development of CP in the WBN/Kob rat.

Acute-Phase Proteins↗

PubMed1999

Conserved T cell receptor complementarity-determining region 3 of ocular T cells in mice with experimental autoimmune uveoretinitis.

PURPOSE: To characterize T cells infiltrating into the ocular tissues of mice with experimental autoimmune uveoretinitis (EAU) immunized with interphotoreceptor retinoid-binding protein (IRBP). METHODS: The T cell receptor (TCR) repertoire on T cells obtained from ocular lesions of EAU mice was analyzed by reverse transcriptase-polymerase chain reaction. The clonotype of the T cells was examined by the single-strand conformation polymorphism (SSCP) method, followed by sequence analysis of the TCR beta-chain complementarity-determining region 3 (CDR3). RESULTS: The repertoire of the TCR BV gene in T cells from inflamed lesions was heterogeneous. SSCP analysis showed accumulation of multiple T cells specifically in ocular tissues of EAU mice, suggesting that these cells were expanded by an antigen-driven stimulation. Junctional sequence analysis demonstrated the presence of highly conserved amino acid sequence motifs (AGTGG, AGD) in CDR3 of BV2-positive T cells. CONCLUSIONS: Our findings suggest that T cells infiltrating into ocular lesions of EAU mice recognize restricted T cell epitopes of IRBP, resulting in autoimmune uveoretinitis.

Amino Acid Sequence↗

PubMed1999

Dopamine D4 gene 7-repeat allele and attention deficit hyperactivity disorder.

OBJECTIVE: Family, twin, and adoption studies show attention deficit hyperactivity disorder (ADHD) to have a substantial genetic component, and some studies have reported an association between ADHD and the dopamine D4 (DRD4) gene. METHOD: The authors recruited 27 triads that comprised an ADHD adult, his or her spouse, and their ADHD child. These triads were assessed for ADHD, and their DNA was genotyped for DRD4 alleles. RESULTS: A multiallelic transmission disequilibrium test suggested an association between ADHD and the DRD4 7-repeat allele. Among family members, the number of 7-repeat alleles predicted the diagnosis of ADHD. CONCLUSIONS: Prior reports of an association between ADHD and DRD4 generalize to families recruited through clinically referred ADHD adults. However, because there are some conflicting studies, further work is needed to clarify the role of DRD4 in the etiology of the disorder.

Adult↗

PubMed1999

[High inducibility of Epstein-Barr virus replication in B lymphocytes in Vogt-Koyanagi-Harada disease].

PURPOSE: The role of Epstein-Barr virus (EBV) reactivation in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease was examined. MATERIAL AND METHODS: Using B lymphocytes obtained from 8 patients with VKH disease and 10 patients with other types of uveitis, immortarized lymphoblast lines were established and infected with EBV. The degree of EBV activation in each lymphoblast line, in the presence and absence of various stimuli, was assessed by measuring the expression of 3 different antigens involved in replication by immunofluorescent staining and western blot analysis. Quantification of EBV DNA in cell culture supernatants was done by polymerase chain reaction. RESULT: Cell lines established from VKH patients expressed more viral antigens that those established from patients with other types of uveitis. There were greater amounts of EBV DNA in the VKH cell lines. CONCLUSION: B lymphocytes from VKH patients may be more susceptible to EBV activation, and the reactivation of EBV may be involved in the pathogenesis of VKH.

Adult↗

PubMed1999

Distribution of thyrotropin releasing hormone receptor type 2 in rats: an immunohistochemical study.

OBJECTIVE: To investigate the organ distribution of thyrotropin releasing hormone receptor (TRHR) type 2 in rats by immunohistochemical method. METHODS: TRHR type 2 was identified immunohistochemically in the rat tissues using specific anti-TRHR antiserum raised in New Zealand white rabbits immunized with a conjugate of synthetic TRHR type 2 (5-23) with bovine serum albumin. Immunohistochemical analysis was performed by avidin-biotin complex method. RESULTS: TRHR type 2 immunoreactivity was visualized in the central nervous system, anterior pituitary, gastric mucosa, Auerbach's and Meissner's nervous branch of the stomach, small intestine and colon, retina amd testis. Significant stain was detected in neural perikarya, axons and dendrites. When using antiserum preincubated with synthetic TRHR type 2(5-23) or anterior pituitary homogenates, no significant stain of anterior pituitary was detected. CONCLUSIONS: These findings suggest that TRHR type 2 is widely distributed and that the method used is valuable in studying the distribution of TRHR type 2 in rats.

Animals↗

PubMed1998

cDNA cloning of mouse and human cholesterol 25-hydroxylases, polytopic membrane proteins that synthesize a potent oxysterol regulator of lipid metabolism.

Oxysterols regulate the expression of genes involved in cholesterol and lipid metabolism and serve as intermediates in cholesterol catabolism. Among the most potent of regulatory oxysterols is 25-hydroxycholesterol, whose biosynthetic enzyme has not yet been isolated. Here, we report the cloning of cholesterol 25-hydroxylase cDNAs from the mouse and human. The encoded enzymes are polytopic membrane proteins of 298 and 272 amino acids, respectively, which contain clusters of histidine residues that are essential for catalytic activity. Unlike most other sterol hydroxylases, cholesterol 25-hydroxylase is not a cytochrome P450, but rather it is a member of a small family of enzymes that utilize diiron cofactors to catalyze the hydroxylation of hydrophobic substrates. The cholesterol 25-hydroxylase gene lacks introns, and in the human it is located on chromosome 10q23. The murine gene is expressed at low levels in multiple tissues. Expression of cholesterol 25-hydroxylase in transfected cells reduces the biosynthesis of cholesterol from acetate and suppresses the cleavage of sterol regulatory element binding protein-1 and -2. The data suggest that cholesterol 25-hydroxylase has the capacity to play an important role in regulating lipid metabolism by synthesizing a co-repressor that blocks sterol regulatory element binding protein processing and ultimately leads to inhibition of gene transcription.

Amino Acid Sequence↗

PubMed1998

Second-site cleavage in sterol regulatory element-binding protein occurs at transmembrane junction as determined by cysteine panning.

In response to sterol deprivation, two sequential proteolytic cleavages release the NH2-terminal fragments of sterol regulatory element-binding proteins (SREBPs) from cell membranes. The fragments translocate to the nucleus where they activate genes involved in cholesterol and fatty acid metabolism. The SREBPs are bound to membranes in a hairpin fashion. The NH2-terminal and COOH-terminal domains face the cytoplasm, separated by two membrane spanning segments and a short lumenal loop. The first cleavage occurs at Site-1 in the lumenal loop. The NH2-terminal fragment is then released by cleavage at Site-2, which is believed to lie within the first transmembrane segment. Here, we use a novel cysteine panning method to identify the second cleavage site (Site-2) in human SREBP-2 as the Leu484-Cys485 bond that lies at the junction between the cytoplasmic NH2-terminal fragment and the first transmembrane segment. We transfected cells with cDNAs encoding fusion proteins with single cysteine residues at positions to the NH2-terminal and COOH-terminal sides of cysteine 485. The NH2-terminal fragments were tested for susceptibility to modification with Nalpha-(3-maleimidylpropionyl)biocytin, which attaches a biotin group to cysteine sulfhydryls. Cysteines to the NH2-terminal side of cysteine 485 were retained on the NH2-terminal fragment, but cysteines to the COOH-terminal side of leucine 484 were lost. Leucine 484 is three residues to the COOH-terminal side of the tetrapeptide Asp-Arg-Ser-Arg, which immediately precedes the first transmembrane segment and is required for Site-2 cleavage.

Amino Acid Sequence↗

PubMed1998

Cleavage of sterol regulatory element-binding proteins (SREBPs) at site-1 requires interaction with SREBP cleavage-activating protein. Evidence from in vivo competition studies.

Sterol regulatory element-binding proteins (SREBPs) are membrane-bound transcription factors that promote lipid synthesis in animal cells. They are embedded in the membranes of the endoplasmic reticulum (ER) in a helical hairpin orientation and are released from the ER by a two-step proteolytic process. Proteolysis begins when the SREBPs are cleaved at Site-1, which is located at a leucine residue in the middle of the hydrophobic loop in the lumen of the ER. Sterols suppress Site-1 cleavage, apparently by interacting with a polytopic membrane protein designated SREBP cleavage-activating protein (SCAP). SREBPs and SCAP are joined together in ER membranes through interaction of their cytoplasmic COOH-terminal domains. Here we use an in vivo competition assay in transfected cells to show that the SREBP.SCAP complex is essential for Site-1 cleavage. Overexpression of the truncated COOH-terminal domains of either SREBP-2 or SCAP disrupted the complex between full-length SREBP-2 and SCAP as measured by co-immunoprecipitation. This resulted in a complete inhibition of Site-1 cleavage that was restored by concomitant overexpression of full-length SCAP. The transfected COOH-terminal domains also inhibited the transcription of a reporter gene driven by an SRE-containing promoter, and this, too, was restored by overexpression of full-length SCAP. We interpret these data to indicate that the SREBP.SCAP complex directs the Site-1 protease to its target in the lumenal domain of SREBP and that disruption of this complex inactivates the Site-1 cleavage reaction.

Amino Acid Sequence↗

PubMed1998

The delayed depolarization in rat cutaneous afferent axons is reduced following nerve transection and ligation, but not crush: implications for injury-induced axonal Na+ channel reorganization.

Two distinct populations of Na+ channels (kinetically fast and slow) are present on the cell bodies and axons of cutaneous afferent neurons; the fast current is increased and the slow current reduced in amplitude following nerve injury. The present study was undertaken to determine if similar changes occur on the axons of these neurons following peripheral nerve injury. The compound action potentials from rat sural nerves were recorded in a sucrose gap chamber. Following application of 4-aminopyridine, a prominent and well-characterized depolarization (the delayed depolarization) followed the action potential. This potential, only present on cutaneous afferent axons, has been correlated with activation of a slow Na+ current. The delayed depolarization was reduced after nerve transection. The refractory period of transmission of the action potential was shortened in the transected nerves, but that of the delayed depolarization was prolonged. The changes were largest when the sural nerve was cut and ligated [control: 38.1 +/- 1.7% (n = 5); injury: 24.5 +/- 2.8% (n = 5), P < 0.05], which prevented reconnection to its peripheral target. When the nerve was crushed and allowed to reestablish peripheral target connections, the delayed depolarization was minimally effected. These results indicate that the changes in Na+ channel organization following peripheral target disconnection observed on cutaneous afferent cell bodies also occur on their axons.

4-Aminopyridine↗

PubMed1998

Suppression of spontaneous uveoretinitis development by non-immunopathogenic peptide immunization.

BALB/c nude mice which are grafted with thymus tissue from fetal F344 rats beneath the renal capsule (hereafter referred to as TG nude mice) spontaneously develop uveoretinitis as well as other organ-localized autoimmune diseases. Active immunization with an interphotoreceptor retinoid-binding protein (IRBP)-derived peptide, amino acids 518-529 (P518-529), induced rapid development and high incidence of uveoretinitis, whereas immunization with another amino acid fragment, 1182-1194 (P1182-1194), inhibited the disease process. P1182-1194- or P518-529-specific T cell lines were established from TG nude mice. Although both were of CD4+ type, P518-529-specific T cells expressed Vbeta8 TCR while Vbeta6 expression was evident in the P1182-1194-specific cells. P518-529-specific T cells produced IL-2 and IFN-gamma, but not IL-4 or IL-10, whereas P1182-1194-specific T cells produced IL-4 and IL-10, but not IL-2 or IFN-gamma Adoptive transfer of these peptide-specific T cells into naive BALB/c nude mice resulted in development of uveoretinitis only in the P518-529 case. Furthermore, mice receiving both T cell types simultaneously did not exhibit uveoretinitis. The results indicate that the amino acid fragment of IRBP, P518-529, is uveitogenic and immunogenic in TG nude mice and induces Th1-type T cells related to uveoretinitis, whereas the amino acid fragment 1182-1194 is immunogenic but not uveitogenic, inducing Th2-type T cells which are involved in inhibition of this pathological response in TG nude mice.

Adoptive Transfer↗

PubMed1998

Intracranial facial nerve neurinoma: surgical strategy of tumor removal and functional reconstruction.

BACKGROUND: Three cases with intracranial facial neurinoma underwent tumor removal and facial nerve reconstruction with or without tympanoplasty. Surgical strategy for each case was tailored to: (1) the site of main tumor mass, (2) its extension along the facial nerve, and (3) involvement of the auditory organs. METHODS: Surgeries adopted in the three cases were: transpetrosal approach with intracranial-intratemporal facial nerve anastomosis, middle fossa and transmastoid approach with intratemporal facial nerve anstomosis and tympanoplasty, and middle fossa and transmastoid approach with intracranial-intratemporal facial nerve anastomosis and tympanoplasty. The greater auricular nerve was used as the nerve graft for all three cases. RESULTS: In the follow-up period of 8-13 months there was no tumor recurrence; facial function was scored 20/90 in modified May's scoring system in each case, but two are still in the process of functional recovery. One of the two cases who underwent tympanoplasty showed complete recovery of hearing within 1 month, and the other showed worsened hearing, which was not serviceable at 3 months postoperatively. CONCLUSION: Systematic surgical approach for tumor removal, facial nerve reconstruction, and auditory reconstruction should be considered in cases with intracranial facial neurinoma due to its varied clinical features.

Aged↗

PubMed1998

Intrahepatic cholangiocarcinoma arising in congenital hepatic fibrosis: report of an autopsy case.

We report an autopsy case of a 60-year-old woman who had congenital hepatic fibrosis with intrahepatic cholangiocarcinoma. A white nodular lesion with a surrounding vague gray area was detected in the right lobe of the liver. Microscopically, most of the nodular lesion was a poorly-differentiated adenocarcinoma. In the surrounding gray area, small bile ducts and bile ductules showed prominent epithelial overgrowth, some of which was composed of dysplasia and well-differentiated adenocarcinoma. The background liver showed the characteristic features of congenital hepatic fibrosis. Immunohistochemically, biliary oncofetal markers (mucin core protein 1 and carcinoembryonic antigen) were more frequently and extensively expressed in poorly-differentiated than well-differentiated adenocarcinoma. This is the 4th reported case of intrahepatic cholangiocarcinoma arising in congenital hepatic fibrosis and suggests that malignant transformation via dysplasia occurs in the abnormal intrahepatic biliary tree of older congenital hepatic fibrosis patients.

Autopsy↗

PubMed1998

Molecular identification of the sterol-regulated luminal protease that cleaves SREBPs and controls lipid composition of animal cells.

The lipid composition of animal cells is controlled by SREBPs, transcription factors released from membranes by sterol-regulated proteolysis. Release is initiated by Site-1 protease (S1P), which cleaves SREBPs in the ER luminal loop between two membrane-spanning regions. To clone S1P, we prepared pCMV-PLAP-BP2, which encodes a fusion protein that contains placental alkaline phosphatase (PLAP) in the ER lumen flanked by cleavage sites for signal peptidase and S1P. In sterol-deprived cells, cleavage by both proteases leads to PLAP secretion. PLAP is not secreted by SRD-12B cells, cholesterol auxotrophs that lack S1P. We transfected SRD-12B cells with pCMV-PLAP-BP2 plus pools of CHO cDNAs and identified a cDNA that restores Site-1 cleavage and PLAP secretion. The cDNA encodes S1P, an intraluminal 1052-amino-acid membrane-bound subtilisin-like protease. We propose that S1P is the sterol-regulated protease that controls lipid metabolism in animal cells.

Alkaline Phosphatase↗

PubMed1998

Intraocular cytokine quantification of experimental autoimmune uveoretinitis in rats.

Elevations of inflammatory cytokines have been implicated in the pathogenesis of experimental autoimmune uveoretinitis (EAU) in rats, although such analysis has relied on indirect methods of assessment such as measurement of mRNA content. In this study, we examined the feasibility of directly measuring cytokine concentrations in intraocular extracts prepared by ultrasonic disruption. Cytokines were measured by ELISA in eyes from EAU-induced Lewis rats immunized with interphotoreceptor retinoid-binding protein (IRBP), and compared to eyes from rats immunized with adjuvant only and from normal rats. Interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-2 (IL-2), interleukin-4 (IL-4), and interleukin-10 (IL-10) were detectable in EAU eyes at near peak inflammation, with IFN-gamma achieving the highest mean concentration (331 pg/ml). In eyes from rats immunized with adjuvant only and in normal eyes, IFN-gamma, TNF-alpha, and IL-10 were nondetectable. IL-2 and IL-4 were detected at significantly lower mean concentrations (32.3 pg/ml and 69.4 pg/ml, respectively) compared to EAU eyes (217 pg/ml and 230 pg/ml, respectively); IL-4 was also detected in eyes from rats immunized with adjuvant alone (141 pg/ml). Thus, a direct method of measuring intraocular cytokine concentrations was successfully applied to reveal an elevation of IFN-gamma, TNF-alpha, IL-2, IL-4, and IL-10 in EAU eyes from rats immunized with IRBP, compared to rats immunized with adjuvant alone and to normal rats. These cytokine elevations reflect the local intraocular environment near peak inflammation, and suggest an important role for these cytokines in the mechanisms of onset and resolution of EAU in rats.

Adjuvants, Immunologic↗

PubMed1998

Effect of type I interferon on experimental autoimmune uveoretinitis in rats.

In order to establish a scientific basis for the potential use of type I interferons (IFNs) in clinical uveitis, we examined the effect of a preparation of IFN-alpha/beta on experimental autoimmune uveoretinitis (EAU). Lewis rats were immunized with bovine interphotoreceptor retinoid-binding protein (IRBP) and given daily intramuscular injections of 10(5) IU mouse natural IFN-alpha/beta. Intraocular inflammation was assessed by slit-lamp biomicroscopy and histopathological examination. Rats treated daily with IFN-alpha/beta starting on the day of IRBP immunization showed decreased intraocular inflammation as well as a slight delay in onset of inflammation when compared to control rats. This effect was also observed to a lesser extent in rats treated during either the induction phase of EAU only, or starting immediately after the onset of inflammation in the effector phase of EAU. Measurement of IRBP-stimulated splenocyte proliferation and serum anti-IRBP antibody subtypes did not reveal a significant difference between IFN-alpha/beta-treated rats and control rats. Measurement of cytokine production by IRBP-stimulated splenocytes in vitro showed significantly decreased TNF-alpha for IFN-alpha/beta-treated rats compared to control, but no difference for IFN-gamma, IL-2, IL-4, and IL-10. These results indicate that systemic administration of IFN-alpha/beta suppresses IRBP-induced EAU in rats, and suggest that such suppression may be mediated in part by a reduction in TNF-alpha production.

Animals↗

PubMed1998

Kinetics of intraocular cytokines in the suppression of experimental autoimmune uveoretinitis by type I IFN.

The systemic administration of IFN-alpha/beta was previously found to suppress inflammation in rats with experimental autoimmune uveoretinitis (EAU); however, an effect on the systemic immune response was not identified. In order to investigate an immunological basis for suppression at the intraocular level, rats immunized with interphotoreceptor retinoid-binding protein (IRBP) were administered daily intramuscular injections of 10(5) IU IFN-alpha/beta and cytokines were measured by ELISA in intraocular extracts prepared by ultrasonification at various timepoints throughout the course of EAU. In control EAU, intraocular concentrations of IFN-gamma were found to be non-detectable on day 8 before the onset of inflammation, significantly elevated on day 12 at peak inflammation (182+/-106 pg/ml), then non-detectable again on day 16 after inflammation had begun to subside. In contrast, intraocular IFN-gamma in IFN-alpha/beta-treated rats remained non-detectable or low at all timepoints. Measurement of intraocular IL-2 revealed no difference between the two groups of rats. Intraocular IL-4 concentrations were elevated in rats treated with IFN-alpha/beta, although this cytokine was also detected in the same range in controls as well as normal rats. Finally, intraocular IL-10 was non-detectable on day 8, significantly elevated at peak inflammation on day 12 (588+/-139 pg/ml), then decreased to low levels on day 16 in control EAU rats, while remaining non-detectable or low in IFN-alpha/beta-treated rats. These results suggest that acute inflammation in IRBP-induced EAU in rats involves both IFN-gamma and IL-10 at the local intraocular level, and that systemic administration of IFN-alpha/beta inhibits EAU via a mechanism that involves suppression of both cytokines.

Animals↗