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Y Sasamoto

Publications and source records attributed to Y Sasamoto.

At least 37 records · Page 2Linked to original sources
PubMed1995

[MHC and non-MHC gene effects on the development of experimental autoimmune uveoretinitis].

Experimental autoimmune uveoretinitis (EAU) can be induced in rats by interphotoreceptor retinoid-binding protein (IRBP), and served as a model for human uveitis. Using IRBP-derived peptide R16, we investigated the MHC and non-MHC genes' effect on the regulation and susceptibility to EAU. EAU-high susceptible LEW (RT1l), EAU-low susceptible WKAH (RT1k), and WKAH.1L rats which carry RT1l and WKAH background were immunized with 2 nmol of R16. One hundred percent of LEW rats developed EAU and 92.9% of WKAH. 1L rats. Only, 18.8% of WKAH rats developed EAU. Among these strains tested, the severity of EAU was 2.06 in LEW, 1.23 in WKAH.1L, and 0.38 in WKAH. R16 evoked substantial proliferative responses in all these strains. The present data suggest that both MHC and non-MHC genes play distinct roles in development of EAU.

Animals↗
PubMed1995

Participation of non-major histocompatibility antigen complex gene in experimental autoimmune uveitis.

It is known that the susceptibility to experimental autoimmune uveitis (EAU) is controlled by both major histocompatibility antigen complex (MHC) and non-MHC genes. In this report, we studied the role of non-MHC genes in the induction of EAU. LEW, WKAH, (LEW x WKAH)F1, and (LEW x WKAH)F2 rats were examined to determine the incidence and severity of EAU induced by immunization with bovine S-antigen (S-Ag). We found that all the LEW rats developed severe EAU within 2 weeks after immunization, but no WKAH rats did. Most of the F1 rats developed mild inflammation in 3-4 weeks after immunization. A quarter of the F2 rats developed EAU within 2 weeks, half of them, in 3-6 weeks after immunization, and the others did not. These findings suggest that only one non-MHC gene controls the susceptibility to S-Ag-induced EAU in rats.

Animals↗
PubMed1994

Immune responses against self-TCR peptides.

Vaccination of rats against the TCR peptide V beta 8.2 (39-59) was reported to inhibit the immunopathogenic process of EAE. Analysis of the immune response to this peptide and several related TCR peptides yielded the following findings: (i) Lewis rats immunized in vivo and challenged in vitro responded with vigorous lymphocyte proliferative responses to peptide V beta 8.2 (39-59) and to three other rat TCR peptides, V beta 8.3 (15-32), V beta 8.3 (39-59), and V beta 14 (39-59). On the other hand, two other rat peptides, V beta 8.2 (18-38) and V beta 8.3 (62-76), were poorly immunogenic. (ii) Rat peptide V beta 8.2 (39-59) was found more immunogenic than its mouse homolog, in both Lewis rats and B10.A mice. A moderate level of cross-reactivity was observed between these two peptide homologs. (iii) Rats of different genetic makeups varied in their response to peptide V beta 8.2 (39-59). A similar pattern of response of the different rats was found with another TCR peptide, V beta 14 (39-59). Hybrids between high and low responder rat strains resembled the high responders in their response to the TCR peptides. (iv) Sensitized lymph node cells as well as lymphocytes of a cell line specific for peptide V beta 8.2 (39-59) failed to respond to T cells that express the V beta 8.2 gene product. This observation is interpreted to indicate that peptide V beta 8.2 (39-59) is a cryptic determinant of the V beta 8.2 protein. Moreover, the data suggest that lymphocytes proliferating against peptide V beta 8.2 (39-59) may not be responsible for the reported inhibition of EAE in rats vaccinated with this peptide.

Amino Acid Sequence↗
PubMed1994

Purification and characterization of gonadotropin I and II from pituitary glands of tuna (Thunnus obesus)

The duality of teleost pituitary gonadotropins was established in an advanced marine fish, the tuna (Thunnus obesus). Two different molecular forms of gonadotropins, designated tGTH I and tGTH II, were isolated from an alcoholic extract of pituitary glands following ion-exchange chromatography and reversed-phase HPLC. Both tGTH I and tGTH II stimulated estradiol-17 beta and testosterone production in tuna ovarian follicles in vitro, although responses to tGTH II were significantly greater than those to tGTH I. Each gonadotropin consisted of alpha- and beta-subunits. tGTH I was stable in acidic conditions, whereas tGTH II dissociated into two subunits after acid treatment. Alpha subunits of tGTH I and tGTH II had identical amino acid sequences of 94 amino acid residues. The tGTH I beta and tGTH II beta consisted of 102 and 115 amino acid residues, respectively, and showed 35% sequence identity. tGTH I beta is structurally more similar to salmon GTH I beta than to salmon GTH II beta, whereas tGTH II beta is more similar to salmon GTH II beta. Thus it is evident that the tuna pituitary gland produces two chemically distinct gonadotropins.

Amino Acid Sequence↗
PubMed1994

Interphotoreceptor retinoid-binding protein derived peptide can induce experimental autoimmune uveoretinitis in various rat strains.

Experimental autoimmune uveoretinitis (EAU) is an intraocular inflammatory disease model induced by retinal specific antigens such as S-antigen and interphotoreceptor retinoid-binding protein (IRBP). The present study was aimed at testing the uveitogenicity of IRBP and an IRBP-derived peptide in various strains of rats with different RT1 (major histocompatibility complex in rats) haplotypes. Immunization with IRBP induced distinct EAU in LEW (RT1l), WKAH (RT1k) W/M (RT1k), LEJ (RT1j), and BUF (RT1b) rats. IRBP also induced a low grade of EAU in SDJ (RT1u), but no disease was detected in TO rats, another strain of the RT1u haplotype. IRBP-derived peptide R16 (aa 1177-1191) induced severe EAU in LEW rats and moderate disease in the WKAH and W/M strains. Immunization with R16 also induced low levels of inflammation in eyes of 75% and 20% of LEJ and BUF rats, respectively, but this peptide did not cause any disease in SDJ and TO rats. Injection of Bordetella pertussis had minimum or no effect on the induction of EAU by peptide R16 in this study. These data thus indicate that peptide R16 can bind to various RT1 molecules in addition to RT1l. Further, our observations support the notion that certain epitopes of IRBP could be uveitogenic in humans with different HLA haplotypes.

Amino Acid Sequence↗
PubMed1994

[A case of multiple sclerosis associated with granulomatous panuveitis].

A case of multiple sclerosis (MS) associated with granulomatous panuveitis was reported. A 45-year-old woman developed diplopia in 1972, at age 24, optic neuritis in 1974 and acute transverse myelopathy in 1981. Subsequently, while being under our care with the clinical diagnosis of MS, right abducens palsy in 1989, deterioration of paraparesis with remission in 1991, and weakness of left arm in 1992 occurred. CSF study revealed high IgG index and brain MRI showed multiple abnormal intensity areas in the deep white matter and periventricular areas bilaterally. On the beginning in March, 1993, she noticed left hazy vision and the ophthalmological examinations revealed marked mutton-fat like keratic precipitates, posterior synechiae, cells and flare in anterior chamber, retinal phlebitis and snow ball vitreous opacity. Granulomatous panuveitis was diagnosed and treated by topical steroid with improvement within two months. During this episode, no neurological deterioration was seen. Granulomatous uveitis in MS was rarely documented in the literatures, but this seems to be more common in women, mildly symptomatic or asymptomatic and responds well to topical steroid treatment.

Female↗
PubMed1994

[Uveitogenicity and immunogenicity of interphotoreceptor retinoid-binding protein-derived peptide R16 in different strains of rats].

Interphotoreceptor retinoid-binding protein (IRBP) can induce experimental autoimmune uveoretinitis (EAU) in different rat strains. This is because IRBP has many epitopes, each of which binds to a specific class II molecule. However, there is the possibility that one epitope can bind to different class II molecules. In this study we attempted to examine this postulate, by checking uveitogenicity and immunogenicity of IRBP-derived peptide R16. We used rat strains LEW, WKAH, SDJ, LEJ, and BUF, which have RT1 haplotype l, k, u, i, and b, respectively. Immunization with R16 caused EAU in LEW (100%), WKAH (75%), SDJ (0%), LEJ (75%), and BUF (19%). We also examined the immunogenicity of R16 by lymphocyte proliferative assay in which lymph node cells from rats of each strain immunized with R16 were stimulated with the immunogen peptide. R16 evoked substantial proliferative responses in LEW, WKAH, LEJ, and BUF, but not in SDJ. An inhibition test with anticlass II monoclonal antibodies showed that OX6 (anti-RT1-B) could inhibit the proliferation against R16, but OX17 (anti-RT1-D) could not. These experiments demonstrated that the same peptide induces the disease and immunity in different strains of rats.

Amino Acid Sequence↗
PubMed1993

Induction of unresponsiveness in adult rats by immunodominant and nondominant peptides.

Intravenous (i.v.) administration of antigens in aqueous solution is an efficient procedure for inducing unresponsiveness in adult animals. Using this procedure, we have compared the unresponsiveness-inducing capacity of an immunodominant and a nondominant peptide derived from the sequence of a retinal antigen, interphotoreceptor retinoid-binding protein (IRBP). The immunodominant peptide, R16, is highly immunogenic in the Lewis rat, while the nondominant peptide, R4, is much less immunogenic and requires higher doses to induce immune response. Pretreatment of Lewis rats with peptides R4 or R16 effectively induced unresponsiveness, shown by the reduced lymphocyte responses following the challenge with the same peptide in adjuvant emulsion. A correlation was found between the doses of each peptide needed to induce immunity or unresponsiveness: both of these doses had to be higher for peptide R4 than for R16. Remarkably, the minimal unresponsiveness-inducing doses of both peptides were lower than those used for the challenge. Pretreatment with the immunodominant peptide, R16, readily inhibited the response to this peptide by lymphocytes from rats challenged with whole IRBP and excessive doses of R16 even affected the response of these rats against whole IRBP. In contrast, R4, which is not recognized by cells of rats challenged with whole IRBP, had no effect on the responses of these rats. The data thus underscore the relationship between immunodominance and unresponsiveness-inducing capacity of peptides and support the notion that the processes of unresponsiveness induction are related to those that produce immunity.

Amino Acid Sequence↗
PubMed1993

[Posterior sub-Tenon's injections of repository corticosteroids in uveitis patients with cystoid macular edema].

Repository corticosteroid was injected into the posterior sub-Tenon's space in 29 cases (39 eyes) of cystoid macular edema (CME) secondary to uveitis. They included 12 cases of Behçet's disease, 7 cases of Sarcoidosis, one case of tuberculous uveitis and 9 cases of etiology unknown uveitis. In some of the patients injections were repeated twice to seven times at intervals of more than 2 weeks. Twenty two of the 39 treated eyes (56.4%) showed visual improvement in at least two lines of visual acuity. Eleven eyes showed no improvement in vision. Most of them had already had bad visual acuity (0.2 or less) before the injections. Complications of the treatment included cataract in 6 eyes, glaucoma in one, and blepharoptosis in one. Injection of repository corticosteroids into the posterior sub-Tenon's space was effective in the treatment of CME secondary to uveitis. However, we have to beware of the complications of this treatment.

Adolescent↗
PubMed1993

[Participation of non-major histocompatibility complex gene in experimental autoimmune uveitis].

It is known that the susceptibility of experimental autoimmune uveitis (EAU) is controlled by both major histocompatibility antigen complex (MHC) and non-MHC genes. In this report, we studied the role of non-MHC gene in the induction of EAU. LEW, WKAH, (LEW x WKAH) F1 and (LEW x WKAH) F2 rats were examined for their incidence and severity to develop EAU by immunization with bovine S-antigen (S-Ag). We found that all LEW rats developed severe EAU within 2 weeks after immunization, but no WKAH rat did. Most F1 rats developed mild inflammation in 3-4 weeks after immunization. A quarter of F2 rats developed EAU within 2 weeks, half of them developed it in 3-6 weeks after immunization, and the others did not. These findings suggest that only one non-MHC gene controls the susceptibility to S-Ag induced EAU in rats.

Animals↗
PubMed1992

The existence of two completely distinct antigenic sites within a decapeptide.

A decapeptide (1182-1191) derived from the bovine interphotoreceptor retinoid-binding protein (IRBP) was found to contain two completely distinct antigenic sites when tested in Lewis rats. One site, localized in sequence 1182-1191, is the core of the immunodominant and highly uveitogenic determinant of IRBP. The second site localizes within sequence 1183-1191 and becomes detectable only when tryptophan at position 1182 is deleted. Lymphocytes sensitized against the first, larger site recognized all longer peptides within sequence 1169-1191, as well as whole IRBP. In contrast, lymphocytes sensitized against the second, short epitope recognized only two peptides, 1184-1191 and (to a lesser degree) 1183-1191. The responses to both sites were restricted by the same major histocompatibility complex (MHC) product (I-A), as shown by monoclonal antibody blocking and by the finding that the lymphocyte response to 1184-1191 was competitively inhibited by peptide 1181-1191. The unique finding of two completely distinct antigenic sites within a decapeptide could be explained by the hypothesis that peptides of the two sites combine with the MHC molecule on antigen-presenting cells by different configurations, thus forming two distinct antigenicities.

Amino Acid Sequence↗
PubMed1992

[The diagnosis of sarcoidosis based on ocular manifestations].

A total of 131 patients with typical ocular manifestations of sarcoidosis were studied. From systemic examinations, 56 cases were confirmed histologically as sarcoidosis, 59 cases were clinically diagnosed as sarcoidosis and 16 cases were not diagnosed as sarcoidosis. There were no differences among the three groups in terms of laterality of eye involvement, sex distribution, ocular findings and prognosis. The only difference was that the age of patients not diagnosed as sarcoidosis was lower than the other two groups. In systemic examinations, patients diagnosed as sarcoidosis histologically or clinically had higher ratios of positive findings of bilateral hilar lymphadenopathy, 67Ga scanning, bronchoalveolar lavage fluid and serum angiotensin converting enzyme than patients who were not diagnosed as sarcoidosis. Some cases of the third group may be diagnosed as sarcoidosis in the future by repeated systemic examinations. The difficulty of diagnosis of sarcoidosis from ocular findings alone was discussed.

Adolescent↗
PubMed1992

Immunomodulation of experimental autoimmune uveoretinitis by intravenous injection of uveitogenic peptides.

Intravenous (IV) injection of antigenic proteins induces specific unresponsiveness, as shown by the diminished response to a challenge with these proteins in complete Freund's adjuvant. This study examined the effect of IV treatment with uveitogenic peptides on the development of experimental autoimmune uveoretinitis (EAU). The peptides used were derived from the sequence of bovine interphotoreceptor retinoid-binding protein (IRBP) and included R16 (sequence, 1177-1191), which is immunodominant and highly uveitogenic, and R4 (sequence, 1158-1180), which is nondominant and weakly uveitogenic. The efficacy of this treatment was found to depend on both the dose used for the IV injection and that used for the challenge. Thus, EAU induced by R16 at a dose of 0.2 nmol/rat was inhibited completely in all rats treated with the peptide at doses of 400 or 133 nmol and partially by the low dose of 5 nmol/rat. However, the EAU induced by a R16 challenge of 40 nmol/rat was inhibited only partially by the high treatment dose of 400 nmol/rat. The IV treatment was found to be effective in inhibiting the EAU induced by peptide R4. A large dose of R4 was needed to induce EAU (40 nmol/rat), and the disease was inhibited completely in all rats treated IV with this peptide at doses of 800, 400, or 133 nmol. In most animals injected with the 44-nmol dose, also, inhibition was complete. These data show that there is a correlation between the doses needed for achieving inhibition and those used for the challenge. The ratios between these doses in all experiments were found within the range 1-20.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1991

Rapid method for preparing a beta-glucan-specific sensitive fraction from Limulus (Tachypleus tridentatus) amebocyte lysate.

By separating Limulus amebocyte lysate by cation-exchange chromatography with an SP-Toyopearl 650C column, a fraction insensitive to endotoxin, yet specifically sensitive to beta-glucan, was successfully obtained in the unadsorbed portion. This fraction showed beta-glucan dose-dependent clotting enzyme activity, although no sensitivity to endotoxin. This beta-glucan-dependent reaction showed no interference in the presence of endotoxin, with the fraction also showing sensitivity towards various kinds of beta-glucan, i.e. curdlan, pachyman, laminaran and lichenan. The sensitivity towards curdlan was approximately 10(-10) g/ml.

Animals↗
PubMed1991

Platelet aggregation induced by uncommon serotypes of Streptococcus sanguis isolated from patients with Behçet's disease.

Uncommon serotypes were tested for their ability to induce aggregation in platelet-rich plasma. Both uncommon and common serotypes induced platelet aggregation in rabbit platelet-rich plasma, but serotonin release was higher with the uncommon serotypes. Aggregation at ATP release varied between uncommon and common serotypes. With human platelet-rich plasma, only uncommon serotypes showed aggregation. Differences in serotype selectivity and the rate of aggregation were noted among platelet donors. About half of the patients with Behçet's disease and 30% of health controls showed platelet aggregation. Plasma from non-responder patients with Behçet's disease inhibited aggregation of healthy responder platelets within 20 min. Thus selective binding of uncommon serotypes of Strep. sanguis to platelets might cause the vasculitis in Behçet's disease.

Adenosine Triphosphate↗
PubMed1991

Microbial sensor system for nondestructive evaluation of fish meat quality.

A microbial sensor system consisting of the bacterium (Alteromonas putrefaciens) immobilized within membranes, a flow cell, an oxygen electrode, peristaltic pumps, a buffer tank, a thermostatically controlled bath and a recorder, was constructed for the nondestructive quality evaluation of bluefin tuna. The chemical compounds on fish meat surfaces which are the indicators of fish meat quality were rapidly determined by using the proposed sensor system. Fish meat quality was determined from the rate of current decrease of the sensor. Good correlations were obtained between fish meat quality and sensor response. One assay could be completed within one minute.

Animals↗
PubMed1991

Regulation of experimental autoimmune uveitis in rats--separation of MHC and non-MHC gene effects.

Experimental autoimmune uveitis (EAU) is an organ-specific autoimmune disease and has served as a model of certain ocular inflammatory conditions in man. The present study was aimed at separating the effects of MHC and non-MHC genes on the development of EAU in the rat. EAU-susceptible LEW (RT1l), EAU-resistant WKAH (RT1k), and WKAH.1L (RT1l) MHC congenic strain of WKAH background rats were immunized with retinal soluble antigen (S-Ag) in Freund's complete adjuvant (FCA). LEW rats showed typical EAU, while neither WKAH nor WKAH.1L congenic rats developed EAU. However, when an additional i.v. injection of Bordetella pertussis was given, all rat strains developed EAU. Furthermore, when immunized with peptide M, an 18-mer synthetic peptide, which corresponds to amino acid positions 303-320 of bovine S-Ag, and given an additional i.v. injection of B. pertussis, LEW and WKAH.1L rats developed EAU, whereas WKAH did not. When ACI (RT1avl), BUF (RT1b), LEJ (RT1j), W (RT1k), F344 (RT1lvl), BN (RT1n), NIG-III (RT1q), TO (RT1t), and SDJ (RT1u) rats were immunized with peptide M or S-Ag and then B. pertussis, all strains developed EAU by immunization with S-Ag plus B. pertussis, but only F344 and NIG-III developed EAU by immunization with peptide M. These findings suggest that susceptibility to EAU in rats is controlled by both MHC and non-MHC genes; and that in the absence of B. pertussis adjuvant, the form of disease induced by native S-Ag in FCA is governed by non-MHC gene(s). However, this effect of non-MHC gene(s) could no longer be observed when the rats were also injected with B. pertussis adjuvant at sensitization.

Amino Acid Sequence↗