Cyclosporin a. Inhibition of experimental autoimmune uveitis in Lewis rats.

Nussenblatt, Robert B.; Rodrigues, Merlyn M.; Wacker, Waldon B.; Cevario, Stanley J.; Salinas-Carmona, Mario C.; Gery, I.

doi:10.1172/jci110138

Cited by 156 publications

(53 citation statements)

References 12 publications

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“…It is therefore possible that lowering serum prolactin levels will enhance the effect of cyclosporine or permit the dose of cyclosporine to be reduced. Previous studies have demonstrated that experimental autoimmune uveitis (EAU)' can be inhibited in the rat by 10 mg/kg per d of cyclosporine (8). This study demonstrates the effect of prolactin suppression by bromocriptine in combination with lower dose cyclosporine (2 mg/kg per d) on EAU induced by S-antigen immunization.…”

Section: Introductionsupporting

confidence: 56%

“…Female and male Lewis rats weighing 175-200 g were used for this series ofexperiments. Bovine retinal S-antigen was prepared as previously described (8). Animals were immunized by injecting into each hind footpad 0.1 cm3 of an emulsion containing 15 Ag of S-antigen in phosphate-buffered saline (PBS) mixed with an equal volume of complete Freund's adjuvant (Gibco, Grand Island, NY) augmented with H37Ra Mycobacterium tuberculosis to a concentration of 2.5 mg/ml.…”

Section: Methodsmentioning

confidence: 99%

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Bromocriptine and low dose cyclosporine in the treatment of experimental autoimmune uveitis in the rat.

Palestine¹,

Muellenberg-Coulombre²,

Kim³

et al. 1987

J. Clin. Invest.

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The immunologic effects of bromocriptine and low dose cyclosporine on experimental autoimmune uveitis (EAU) induced in Lewis rats by S-antigen immunization were studied. Rats treated with a sub-optimal dose (low dose) of cyclosporine (2 mg/kg per d), bromocriptine (1.8 mg/kg per d), or both drugs were compared with untreated rats in regard to the development of EAU, lymphocyte proliferative responses, and anti-S-antigen serum antibodies. Bromocriptine alone decreased the incidence of EAU only in female rats (P < 0.01), did not effect the lymphocyte proliferative response, but did significantly decrease antibody titers in both males (P < 0.004) and females (P < 0.0005). Low dose cyclosporine also partially decreased the incidence of EAU in female rats, but did not decrease antibody titers or lymphocyte proliferative responses. Bromocriptine plus low-dose cyclosporine led to more marked decreases in the incidence of EAU and anti-S-antigen antibody titers as well as in the lymphocyte proliferative assay (P < 0.01 for males, P < 0.0005 for females). This study suggests that bromocriptine can enhance the immunosuppression of low dose cyclosporine.

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Section: Introductionsupporting

confidence: 56%

Section: Methodsmentioning

confidence: 99%

Bromocriptine and low dose cyclosporine in the treatment of experimental autoimmune uveitis in the rat.

Palestine¹,

Muellenberg-Coulombre²,

Kim³

et al. 1987

J. Clin. Invest.

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“…Cyclosporine, with its specific immunomQtfularory action (13)(14)(15) and TABLE 1 its efficacy and relat ive safety in comparison to other immu nosu ppressivc agents, particularly in organ t ransplantation ( 15,16), and its effective prevention of autoimmunity in an imal models ( 17,18), has prompted its experimental use in a series of autoimmu ne d isease:, in man ( 19), including Croh n 's disease. Preliminary stud ies with Crohn's disease have been encouraging (20)(21)(22).…”

Section: Rohn's D Isease Is a Chronicmentioning

confidence: 99%

Open Trial of Cyclosporine in Patients with Severe Active Crohn's Disease Refractory to Conventional Therapy

Peltekian

Williams

Macdonald

et al. 1988

Canadian Journal of Gastroenterology

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Fifteen pat ients with severe active Crohn's disease, refra ccory to conventional therapy, were given a 16 week cou rse of cyclosporine ar an initial oral daily dose of 10 mg/kg, adjusted to ma intain cyclosporine scrum trough levels between 100 and 200 ng/m l. Five patients withdrew early because of side effects, poor absorption or noncompliance. T he remaining 10 patients all improved within four weeks as measured by three d iffe rent clinical indices: Crohn's Disease Activity Index, Simple Index of Crohn's Disease A ctivity and Mean Score of Therapeutic Goals (MSTG). Seven patients maintained th is initial improvement and prcdnisone was either reduced or discontinued. Four of these seven patients relapsed with in four wceb of stopping cyclosporine, and three remain in remission after 75 ± 2 weeks. S ide effects were minor and easily reversible. When the various clinical and labo ratory indices were compared, MSTG was found to be the most useful index fo r the assessment of therapy. Cyclosporine appears to be a safe and effective therapy in patients with severe active Crohn's disease refractory to conventional therapy. Ca n J Gastroenterol 1988; 2(1): 5-11

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“…In susceptible strains of rodents, injection of some of these proteins causes autoimmune diseases characterized by an inflammation of the uveal tract and retina, resulting in subsequent loss ofphotoreceptor cells (15,16). Arrestin (also known as S-antigen, a soluble protein of 48 kDa) is one ofthe retina-dominant proteins that induces autoimmune uveitis, a T-celi-mediated disease (17)(18)(19)(20). In humans, intraocular inflammation may resemble experimental autoimmune uveoretinitis, and some patients show T-cell responses to either bovine or human arrestin (21).…”

mentioning

confidence: 99%

Beta-arrestin and arrestin are recognized by autoantibodies in sera from multiple sclerosis patients.

Ohguro

Chiba

Igarashi

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Multiple sclerosis (MS), one of the most common chronic neurologic diseases, is characterized by the presence of multiple plaques of demyelination throughout the central nervous system. Although the etiology of the disea has not been established, it is believed to involve autoimmune mechanisms. We have examined sera from patients with MS for the presence of antibodies to antigens from brain and retina. Immunoblot analysis of the soluble fraction of proteins from bovine brain revealed a prominent band at 45 kDa stained with sera of 8-14 patients with MS. In two patients with MS, serum antibody titers during relapse were higher compared with those when the patients were in remission. These antibodies were undetectable in cerebrospinal fluid of our MS patients and additionally were absent in sera of patients with other neurological diseases and normal control subjects. Furthermore, immunoblot analysis of the soluble fraction from bovine retinal rod outer segments revealed a prominent protein band at 48 kDa stained with MS sera. This antigen was purified to homogeneity from bovine retinal outer segments and identified as arrestin. Additionaly, sera from MS patients reacted with purified 03arrestin 1, a 45-kDa protein homologous to arrestin that is found in various tissues. Using limited proteolysis of arrestin and a competitive ELISA test with a synthetic peptide, we identified the recognition site(s) for antibodies in sera of MS patients at a dominant immunogenic site on arrestin located at the C-terminal region of the molecule. We suggest that the presence of circulating antibodies reactive with -arrestin or arrestin may be related to the course of MS progression.

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Cyclosporin a. Inhibition of experimental autoimmune uveitis in Lewis rats.

Cited by 156 publications

References 12 publications

Bromocriptine and low dose cyclosporine in the treatment of experimental autoimmune uveitis in the rat.

Bromocriptine and low dose cyclosporine in the treatment of experimental autoimmune uveitis in the rat.

Open Trial of Cyclosporine in Patients with Severe Active Crohn's Disease Refractory to Conventional Therapy

Beta-arrestin and arrestin are recognized by autoantibodies in sera from multiple sclerosis patients.

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