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      Mouse Models of Experimental Autoimmune Uveitis

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          Abstract

          The mouse model of experimental autoimmune uveitis, induced by immunization of mice with the retinal protein IRBP, was developed in our laboratory 20 years ago and published in 1988. Since that time it has been adopted by many investigators and has given rise to many studies that helped elucidate genetic influences, dissect the basic mechanisms of pathogenesis and test novel immunotherapeutic paradigms. The current overview will summarize the salient features of the experimental autoimmune uveitis model and discuss its mechanisms.

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          Defective antioxidative activity of small dense HDL3 particles in type 2 diabetes: relationship to elevated oxidative stress and hyperglycaemia.

          B Hansel, E Nobécourt, Fae Chapman … (2005)
          Elevated oxidative stress, hyperglycaemia, and dyslipidaemia involving low levels of HDL particles are key proatherogenic factors in type 2 diabetes mellitus. We examined the relationship of oxidative stress, and the degree of glycaemia and triglyceridaemia, to antioxidative function of HDL particle subspecies in type 2 diabetes. Five HDL subfractions (2b, 2a, 3a, 3b, 3c) were isolated by density gradient ultracentrifugation from well-controlled type 2 diabetic subjects (n=20) and normolipidaemic, non-diabetic controls (n=10). Specific antioxidative activity (capacity to protect LDL from oxidation on a unit particle mass or on a particle number basis), chemical composition and enzymatic activities were measured in each subfraction. Systemic oxidative stress was assessed as plasma levels of 8-isoprostanes. Specific antioxidative activity of small dense HDL3b and 3c particles in diabetic patients was significantly diminished (up to -47%, on a particle mass or particle number basis) as compared with controls. Plasma 8-isoprostanes were markedly elevated (2.9-fold) in diabetic patients, were negatively correlated with both specific antioxidative activity of HDL3 subfractions and plasma HDL cholesterol (HDL-C) levels, and were positively correlated with glycaemia and triglyceridaemia. Paraoxonase 1 activity was consistently lower in diabetic HDL subfractions and was positively correlated with HDL3 antioxidative activity. The altered chemical composition of diabetic HDL3 subfractions (core cholesteryl ester depletion, triglyceride enrichment) was equally correlated with diminished antioxidative activity. Antioxidative activity of small dense HDL is deficient in type 2 diabetes, is intimately linked to oxidative stress, glycaemia and hypertriglyceridaemia and primarily reflects abnormal intrinsic physicochemical properties of HDL particles.
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            High pre-beta1 HDL concentrations and low lecithin: cholesterol acyltransferase activities are strong positive risk markers for ischemic heart disease and independent of HDL-cholesterol.

            Boris L. Vaisman, Evandro Muniz, Maureen Sampson … (2010)
            We hypothesized that patients with high HDL-cholesterol (HDL-C) and ischemic heart disease (IHD) may have dysfunctional HDL or unrecognized nonconventional risk factors. Individuals with IHD (Copenhagen University Hospital) and either high HDL-C (n = 53; women >or=735 mg/L; men >or=619 mg/L) or low HDL-C (n = 42; women
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              The relationship between high density lipoprotein subclass profile and plasma lipids concentrations

              Li Tian, Mingde Fu (2010)
              HDL particles posses multiple antiatherogenic activities and the identification and differentiation of individual HDL subclasses may be useful in documentation and understanding of metabolic changes of different HDL subclasses. The major plasma lipids exist and are transported in the form of lipoprotein complexes. Hence, alterations in plasma lipids levels can interfere with the composition, content, and distribution of plasma lipoprotein subclasses that affect atherosclerosis risk. The research review major discussed the relationship between plasma lipids levels and HDL subclasses distribution. The general shift toward smaller size of HDL particle size in HTG, HCL and MHL subjects, and the changes were more prominent with the elevation of TG and TC levels which imply that HDL maturation might be abnormal and RCT pathway might be weaken, and these changes were more seriously in MHL subjects. Plasma contents of small sized HDL particles significantly higher, whereas those of large sized HDL particles were significantly lower with elevation of TG/HDL-C and TC/HDL-C ratios. Increased in the TC/HDL-C ratio alone did not influence the distributions of HDL subclasses significantly when the TG/HDL-C ratio was low (TG/HDL-C ≤ 2.5). Hence, the TG/HDL-C ratio might be more sensitive to reflect the alteration of HDL subclass distribution than the TC/HDL-C ratio. In LDL-C/HDL-C ≤ 2.3 group, the pattern of distribution in HDL subclass was in agreement with the normolipidemic subjects. Moreover, considering the relative ease of measuring TC/HDL-C, TG/HDL-C and LDL-C/HDL-C ratios, as opposed to measuring HDL subclasses, these 3 ratios together may be a good indicator of HDL subclass distribution. The protective effect of increased apoA-I levels against the reduction of HDL2b caused by elevated TG concentration. On one hand, plasma HDL-C and apoA-I appear to play a coordinated role in the assembly of HDL particles and the determination of their contents among the total subjects. On the other hand, the apoA-I level might be a more powerful factor than HDL-C to influence the distribution of HDL subclasses in hyperlipidemic subjects. At the same time, from point of HDL subclasses distribution, the plasma lipids, apos concentrations and apos ratios should be considered while assessing the CHD risk. Abnormality of HDL subclasses distribution may result in accelerated atherosclerosis, therapeutic normalization of attenuated antiatherogenic HDL function in terms of both particle number and distribution of HDL particles is the target of innovative pharmacological approaches to large-sized HDL particles rising, including enhanced apoA-I levels.
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                Author and article information

                Journal
                Journal ID (publisher-id): ORE
                Journal ID (nlm-ta): Ophthalmic Res
                Journal ID (doi): 10.1159/issn.0030-3747
                Title: Ophthalmic Research
                Publisher: S. Karger AG
                ISBN: 978-3-8055-8584-2
                ISBN: 978-3-8055-8585-9
                ISSN (Print): 0030-3747
                ISSN (Electronic): 1423-0259
                Publication date Subscription-year: 2008
                Publication date (Print): April 2008
                Publication date (Electronic): 18 April 2008
                Volume: 40
                Issue: 3-4
                Pages: 169-174
                Affiliations
                Laboratory of Immunology, NEI, NIH, Bethesda, Md., USA
                Article
                Publisher ID: 119871 Pmcid ID: PMC2735820 Other ID: Ophthalmic Res 2008;40:169–174
                DOI: 10.1159/000119871
                PMC ID: PMC2735820
                PubMed ID: 18421234
                SO-VID: 5fb27a83-2393-4e1a-9f50-16c8e6f390f4
                Copyright © © 2008 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 2, Tables: 1, References: 23, Pages: 6
                Categories
                Subject: Paper

                ScienceOpen disciplines: Vision sciences,Ophthalmology & Optometry,Pathology
                Keywords: Uveitis, mouse,Th17,Uveoretinitis,Autoimmune disease,Th1
                Data availability:
                ScienceOpen disciplines: Vision sciences, Ophthalmology & Optometry, Pathology
                Keywords: Uveitis, mouse, Th17, Uveoretinitis, Autoimmune disease, Th1

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