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Autoimmune Pathogenesis (autoimmune + pathogenesis)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Immunopathogenesis of cholestatic autoimmune liver diseases

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2001
J. Medina
Primary biliary cirrhosis and primary sclerosing cholangitis are well recognized chronic cholestatic liver diseases that are considered to have an autoimmune basis. Recent progress in the study of autoimmune liver diseases has improved the recognition and characterization of these conditions. An important component of this progress has been the identification of liver disease-associated autoantibodies and their respective target antigens, and the development of specific assays for these autoantibodies. In addition, some nonhumoral immunological findings imply an involvement of specific immunopathogenic mechanisms in the development of these conditions. Furthermore, immunogenetic factors associated with increased susceptibility to some of these diseases have been identified. This article reviews the most relevant information relating to the postulated autoimmune pathogenesis of these diseases, with special emphasis on their associated humoral and cellular immunological abnormalities and immunopathogenetic factors. Some of the remaining important unresolved issues relating to the pathogenesis of these diseases, that need to be addressed in further research, are highlighted. [source]

A human-specific TNF-responsive promoter for Goodpasture antigen-binding protein

FEBS JOURNAL, Issue 20 2005
Froilán Granero
The Goodpasture antigen-binding protein, GPBP, is a serine/threonine kinase whose relative expression increases in autoimmune processes. Tumor necrosis factor (TNF) is a pro-inflammatory cytokine implicated in autoimmune pathogenesis. Here we show that COL4A3BP, the gene encoding GPBP, maps head-to-head with POLK, the gene encoding for DNA polymerase kappa (pol ,), and shares with it a 140-bp promoter containing a Sp1 site, a TATA-like element, and a nuclear factor kappa B (NF,B)-like site. These three elements cooperate in the assembly of a bidirectional transcription complex containing abundant Sp1 and little NF,B that is more efficient in the POLK direction. Tumour necrosis factor cell induction is associated with Sp1 release, NF,B recruitment and assembly of a complex comparatively more efficient in the COL4A3BP direction. This is accomplished by competitive binding of Sp1 and NF,B to a DNA element encompassing a NF,B-like site that is pivotal for the 140-bp promoter to function. Consistently, a murine homologous DNA region, which contains the Sp1 site and the TATA-like element but is devoid of the NF,B-like site, does not show transcriptional activity in transient gene expression assays. Our findings identify a human-specific TNF-responsive transcriptional unit that locates GPBP in the signalling cascade of TNF and substantiates previous observations, which independently related TNF and GPBP with human autoimmunity. [source]

Can antiglycolipid antibodies present in HIV-infected individuals induce immune demyelination?

NEUROPATHOLOGY, Issue 4 2000
Steven Petratos
Of the eight clinically defined neuropathies associated with HIV infection, there is compelling evidence that acute and chronic inflammatory demyelinating polyneuropathy (IDPN) have an autoimmune pathogenesis. Many non-HIV infected individuals who suffer from sensorymotor nerve dysfunction have autoimmune indicators. The immunopathogenesis of demyelination must involve neuritogenic components in myelin. The various antigens suspected to play a role in HIV-seronegative IDPN include (i) P2 protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM1); (iv) galactocerebroside (GalC); and (v) glycoproteins or glycolipids with the carbohydrate epitope glucuronyl-3-sulfate. These glycoproteins or glycolipids may be individually targeted, or an immune attack may be raised against a combination of any of these epitopes. The glycolipids, however, especially GalS, have recently evoked much interest as mediators of immune events underlying both non-HIV and HIV-associated demyelinating neuropathies. The present review outlines the recent research findings of antiglycolipid antibodies present in HIV-infected patients with and without peripheral nerve dysfunction, in an attempt to arrive at some consensus as to whether these antibodies may play a role in the immunopathogenesis of HIV-associated inflammatory demyelinating polyneuropathy. [source]

Paraneoplastic neurological syndromes , patients' cohort profile in the Czech Republic

ACTA NEUROLOGICA SCANDINAVICA, Issue 2 2001
toura
Reported paraneoplastic neurological syndromes (PNS) are rare disabling neurological diseases with supposed autoimmune pathogenesis. The aims of this study were to evaluate frequency, clinical course and therapeutic response in the cohort of PNS positive patients (n=10) in the Czech Republic for the first time. Second, we determined the presence and distribution of oligoclonal IgG bands (OB IgG) in PNS and compared the clinical and laboratory features of OB IgG positive and negative patients. A total of 2355 suspicious serum and/or CSF samples were screened by immunofluorescence and immunohistochemistry with definite confirmation by Western blot. OB IgG were detected by isoelectric focusing and immunoenzymatic staining and clinical status was scored according to modified Rankin scale (RS). Four patients had anti-Yo antibody, ovarian cancer and the score in range (2,5) on RS. Five patients had anti-Hu antibody, small cell lung cancer (SCLC), prostate cancer and the score between 1,4 grade on RS. One patient with SCLC and anti-Ri antibody had grade 2. Five of 10 patients with PNS had positive OB IgG and average value 4.2 on RS comparing with negative OB IgG patients with average value 2.6. Finally, we add well-defined cohort of PNS patients to emerging European profile of PNS and conclude that the presence of OB IgG in PNS seems to reflect enhanced immune response with more severe neurological damage and clinical course. [source]