5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      A review of immunologic diseases of the dog

      research-article
      *
      Veterinary Immunology and Immunopathology
      Elsevier Science B.V.

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The following review is based on notes used in the teaching of clinical immunology to veterinary students. Immune diseases of the dog are placed into six different categories: (1) type I or allergic conditions; (2) type II or auto- and allo-antibody diseases; (3) type III or immune complex disorders; (4) type IV or cell-mediated immune diseases; (5) type V conditions or gammopathies; and (6) type VI or immunodeficiency disorders. Separate discussions of transplantation immunology and the use of drugs to regulate unwanted immune responses are also included.

          Related collections

          Most cited references318

          • Record: found
          • Abstract: found
          • Article: not found

          Independent regulation of sterol regulatory element-binding proteins 1 and 2 in hamster liver.

          Two sterol regulatory element-binding proteins (SREBPs, designated SREBP-1 and SREBP-2), each approximately 1150 amino acids in length, are attached to membranes of the endoplasmic reticulum and nuclear envelope in human and hamster tissue culture cells. In the absence of sterols, soluble fragments of approximately 470 amino acids are released from both proteins by proteolytic cleavage. The soluble fragments enter the nucleus, where they bind to sterol regulatory elements in the promoters of genes encoding the low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl CoA synthase, thereby activating transcription. Proteolytic processing of both SREBPs is blocked coordinately by sterol overloading and enhanced coordinately when sterols are depleted by treatment with an inhibitor of cholesterol synthesis. In contrast to these findings in cultured cells, the current data show that SREBP-1 and -2 are not coordinately regulated in hamster liver. In untreated animals the soluble fragment of SREBP-1, but not of SREBP-2, was detected by immunoblotting of a liver nuclear extract. Depletion of sterols by treatment with a bile acid-binding resin (colestipol) and a cholesterol synthesis inhibitor (mevinolin) led to a marked increase in the nuclear form of SREBP-2 and a reciprocal decline in the nuclear form of SREBP-1. These findings suggest that SREBP-1 is responsible for basal transcription of the low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl CoA synthase genes in hamster liver and that SREBP-2 is responsible for the increased transcription that follows sterol depletion with a bile acid-binding resin and a cholesterol synthesis inhibitor.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Acute eosinophilic pneumonia. A summary of 15 cases and review of the literature.

            Idiopathic acute eosinophilic pneumonia (AEP) is an acute febrile illness that may be mistaken for an infectious pneumonia. Patients are often young and otherwise healthy. Clues to considering this disorder in a differential diagnosis include the acuity and severity of the clinical presentation and an initial chest X-ray with diffuse infiltrates, often interstitial, and the presence of Kerley B lines and/or evidence of pleural fluid. The diagnosis can be made through examination of bronchoalveolar lavage fluid in most cases, with careful exclusion of other similar eosinophilic lung disease. Although it can lead to life-threatening respiratory failure, AEP is easily treatable with corticosteroids. This disease has not been reported to recur in any patients to this point.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Expansion of unusual CD4+ T cells in severe rheumatoid arthritis.

              The repertoire of T cells in patients with rheumatoid arthritis (RA) is characterized by clonal expansion of selected CD4+ T cells, which are autoreactive and lack the expression of the functionally important CD28 molecule. The goal of this study was to determine the contribution of these unusual lymphocytes to the disease process. RA patients (n = 108) and normal controls (n = 53) were examined for the expression of CD4+ CD28- T cells by 2-color fluorescence-activated cell sorter analysis. Clinical data were ascertained by retrospective chart review. The frequencies of CD4+ CD28- T cells displayed a bimodal distribution, defining carriers and noncarriers in normal subjects and RA patients. In longitudinal studies, the noncarrier and carrier phenotypes were stable over time. Carriers of CD4+ CD28- T cells accumulated in the RA population (64% versus 45%; P = 0.02). The expansion of CD4+ CD28- T cells correlated with extraarticular involvement, but not with disease duration, antirheumatic treatment, or severity of joint destruction. The patient subsets with nodular disease (P = 0.02) and rheumatoid organ disease (P = 0.04) had the highest proportion of CD4+ CD28- T cell carriers. The size of the CD4+ CD28- compartment correlated with extraarticular progression of RA (P = 0.001 in nodular RA, P = 0.003 in rheumatoid organ disease). The bimodality of distribution of CD4+ CD28- T cell frequencies is compatible with genetic control of the generation of these unusual T cells. In RA patients, CD4+ CD28- T cells are not an epiphenomenon of the disease process, but predispose patients to developing inflammatory lesions in extraarticular tissues.
                Bookmark

                Author and article information

                Journal
                Vet Immunol Immunopathol
                Vet. Immunol. Immunopathol
                Veterinary Immunology and Immunopathology
                Elsevier Science B.V.
                0165-2427
                1873-2534
                17 September 1999
                2 August 1999
                17 September 1999
                : 69
                : 2
                : 251-342
                Affiliations
                Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA
                Author notes
                [* ]Tel.: +1-530-752-7402; fax: +1-530-752-0414.
                Article
                S0165-2427(99)00059-8
                10.1016/S0165-2427(99)00059-8
                7119806
                10507310
                b8fd549a-31b7-439d-ba08-c1738a01fd22
                Copyright © 1999 Elsevier Science B.V. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Categories
                Article

                Veterinary medicine
                Veterinary medicine

                Comments

                Comment on this article