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Biomedical subjects

Robert Nussenblatt

Publications and source records attributed to Robert Nussenblatt.

7 recordsLinked to original sources
PubMed2006

Advances in immunology: from bench to bedside--a symposium at the 2005 Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS), Boston, MA, USA.

The American Uveitis Society sponsored a symposium at the recent 2005 Annual FOCIS meeting in Boston, MA, USA, that was organized by the authors of this report. The symposium was designed to bring together several leaders in the broad field of immunology and investigators in ocular immunology to discuss three interrelated areas of interest: (i) animal models of ocular inflammation; (ii) interface of innate and adaptive immunity; and (iii) immune regulation. A brief summary of the salient points of the symposium is given.

Adaptation, Physiological↗
PubMed2004

Orally and nasally induced tolerance studies in ocular inflammatory disease: guidance for future interventions.

The induction of both oral and nasal tolerance has been used in both experimental models of ocular disease and clinically. Initial work centered around the abrogation of experimental autoimmune uveitis using either one or two whole uveitogenic antigens. Other models of ocular disease have included a corneal transplant model, demonstrating that feeding splenocytes from the donor strain of rats enhanced corneal engraftment. Fragments of pertinent antigens have been shown to alter the expression of experimental uveitis and possibly human disease. A randomized, masked study in uveitis provided valuable information for future studies, demonstrating that single antigen feeding provided far better protection than the feeding of multiple antigens. This review will deal with animal and human studies in the treatment of ocular inflammatory disease with the goal of extracting from past experience how to construct a future study in humans.

Administration, Intranasal↗
PubMed2003

Toxoplasmosis transmitted to a newborn from the mother infected 20 years earlier.

PURPOSE: To present a case of congenital toxoplasmosis in a newborn whose mother had a 20-year history of a chorioretinal macular scar and positive serology for toxoplasmosis. DESIGN/METHODS: Case report. SETTING/RESULTS: A 38-year-old woman who had been treated for ocular toxoplasmosis 20 years earlier delivered a newborn who presented with a focal necrotizing retinochoroiditis characteristic of toxoplasmosis, as well as positive immunoglobulin (Ig) G and M serology for toxoplasmosis. The workup was negative for other entities. CONCLUSION: This case suggests that women with old retinal scars due to toxoplasmosis and long-standing IgG antibodies to toxoplasmosis are also at risk of transmitting this disease to the fetus.

Adult↗
PubMed2003

Antigenic specificity of immunoprotective therapeutic vaccination for glaucoma.

PURPOSE: To investigate the antigenic specificity of the immune neuroprotective mechanism that can protect retinal ganglion cells (RGCs) against death caused by high intraocular pressure (IOP). METHODS: A unilateral increase in IOP was induced in rats by argon laser photocoagulation of the episcleral veins and limbal plexus. Rats with high IOP were immunized with glatiramer acetate (Cop-1, a synthetic copolymer) or with myelin-derived or uveitogenic peptides. When the steroid drug methylprednisolone was used, it was administered intraperitoneally every other day for 12 days. RESULTS: Vaccination with myelin-derived peptides that reside in the axons failed to protect RGCs from death caused by high IOP. In contrast, IOP-induced RGC loss was reduced by vaccination with R16, a peptide derived from interphotoreceptor retinoid-binding protein, an immunodominant antigen residing in the eye. The benefit of protection against IOP-induced RGC loss outweighed the cost of the monophasic experimental autoimmune uveitis (EAU) that transiently developed in a susceptible rat strain. Treatment with methylprednisolone alleviated the disease symptoms, but caused further loss of RGCs. Cop-1 vaccination was effective in both EAU-resistant and EAU-susceptible strains. CONCLUSIONS: To benefit damaged neurons, immune neuroprotection should be directed against immunodominant antigens that reside in the site of damage. In a rat model of high IOP, RGCs can benefit from vaccination with peptides derived from proteins that are immunodominant in the eye but not from myelin-associated proteins. This suggests that the site of primary degeneration in IOP-induced RGC loss is in the eye. Cop-1 vaccination apparently circumvents the site-specificity barrier and provides protection without risk of inducing autoimmune disease.

Animals↗