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  • Oxford University Press (OUP)  (4)
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  • Oxford University Press (OUP)  (4)
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  • 1
    Online Resource
    Online Resource
    Autoantibodies against complement receptor 1 (CD35) in SLE, liver cirrhosis and HIV-infected patients
    Oxford University Press (OUP) ; 2003
    In:  Clinical and Experimental Immunology Vol. 131, No. 1 ( 2003-01-07), p. 174-181
    Details
    In: Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 131, No. 1 ( 2003-01-07), p. 174-181
    Abstract: The acquired loss of CR1 (CD35) on erythrocytes in specific autoimmune diseases and chronic infections may be due to autoAb against CR1. An ELISA using rCR1 was established to measure antiCR1 IgG autoAb. Plasma containing alloAb to polymorphism on CR1 (Knops blood group Ab) reacted strongly against rCR1 and were used as positive controls. AntiCR1 Ab was found in 3/90 (3·5%) plasma samples from healthy blood donors. The binding of these Ab was not inhibited by high salt concentrations. AntiCR1 Ab were present in the IgG fractions of plasma, and they bound to rCR1 on Western Blot. Affinity chromatography on rCR1-sepharose depleted the plasma of antiCR1, and the acid-eluted fractions contained the antiCR1 Ab. An increased frequency of antiCR1 autoAb was found in patients with SLE (36/78; 46%), liver cirrhosis (15/41; 36%), HIV infection (23/76; 30%) (all P  & lt; 0·0001), and in patients with anticardiolipin Ab (4/21; 19%, P  & lt; 0·01) multiple sclerosis (7/50; 14%, P  & lt; 0·02), and myeloma (autoAb (8/56; 14%, P  & lt; 0·02), but not in those with acute poststreptococcal glomerulonephritis (1:32; 3%). Because C1q binds to CR1, antiC1q Ab were analysed in the same patients. There was no correlation between levels of antiC1q and antiCR1 autoAb. In HIV patients, levels of antiCR1 did not correlate with low CR1 levels expressed on erythrocytes or soluble CR1 in plasma. The binding of antiCR1 autoAb to rCR1 fixed on ELISA plates was not inhibited by soluble rCR1 or by human erythrocyte CR1, in contrast to alloAb and one SLE serum, which induced partial blockade. Thus, antiCR1 autoAb recognize mostly CR1 epitope(s) not present on the native molecule, suggesting that they are not directly involved in the loss of CR1. Rather antiCR1 autoAb might indicate a specific immune response to denatured CR1.
    Type of Medium: Online Resource
    ISSN: 0009-9104 , 1365-2249
    URL: Article
    DOI: 10.1046/j.1365-2249.2003.02045.x
    RVK:
    XA 36770
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2003
    detail.hit.zdb_id: 2020024-9
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Yo antibodies in ovarian and breast cancer patients detected by a sensitive immunoprecipitation technique
    Oxford University Press (OUP) ; 2006
    In:  Clinical and Experimental Immunology Vol. 144, No. 1 ( 2006-02-16), p. 53-58
    Details
    In: Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 144, No. 1 ( 2006-02-16), p. 53-58
    Abstract: Onconeural antibodies are found in patients with cancer and are associated with paraneoplastic neurological syndromes (PNS). The objective of the present study was to assess the frequency of Yo antibodies in ovarian and breast cancer using a sensitive immunoprecipitation technique, and to look for any association of Yo antibodies with neurological symptoms and prognostic factors. A multiwell adapted fluid-phase immunoassay using radiolabelled recombinant cerebellar degeneration related protein (cdr2), produced by coupled in vitro transcription/translation was used for the detection of Yo antibodies. This technique combines high specificity and sensitivity with high sample analysing capacity for the antibody in question. Sera or EDTA-blood from 810 ovarian (n = 557) and breast cancer (n = 253) patients were analysed for Yo antibodies by immunoprecipitation, as well as immunofluorescence and immune blots. Two hundred healthy blood donors and sera from 17 patients with paraneoplastic cerebellar degeneration and Yo antibodies served as controls. Immunoprecipitation was more sensitive in detecting Yo antibodies than immunofluorescence and immune blots. The prevalence of Yo antibodies was 13/557 (2·3%) in ovarian cancer and 4/253 (1·6%) in breast cancer using immunoprecipitation. Yo antibodies were not correlated with specific histological subgroups. The Yo index of ovarian cancer patients in FIGO stage IV was higher compared to FIGO stage I-III. The prevalence of Yo antibodies was 3 times higher in patients with stage III breast cancer than in stage I and II. Only 2/17 (11·8%) patients with Yo antibodies detected during the screen of 810 cancer patients had PNS. The results show that the prevalence of Yo antibodies is low in ovarian and breast cancer. Yo antibodies may be associated with advanced cancer, but less often with PNS.
    Type of Medium: Online Resource
    ISSN: 1365-2249 , 0009-9104
    URL: Article
    DOI: 10.1111/j.1365-2249.2006.03031.x
    RVK:
    XA 36770
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2006
    detail.hit.zdb_id: 2020024-9
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Systemic complement activation following human acute ischaemic stroke
    Oxford University Press (OUP) ; 2004
    In:  Clinical and Experimental Immunology Vol. 137, No. 1 ( 2004-06-08), p. 117-122
    Details
    In: Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 137, No. 1 ( 2004-06-08), p. 117-122
    Abstract: The brain tissue damage after stroke is mediated partly by inflammation induced by ischaemia–reperfusion injury where the complement system plays a pivotal role. In the present study we investigated systemic complement activation and its relation to C-reactive protein (CRP), a known complement activator, and other inflammatory mediators after acute ischaemic stroke. Sequential plasma samples from 11 acute stroke patients were obtained from the time of admittance to hospital and for a follow-up period of 12 months. Nine healthy gender- and age-matched subjects served as controls. The terminal SC5b-9 complement complex (TCC), CRP, soluble adhesion molecules (L-, E- and P- selectin, ICAM, VCAM) and cytokines [tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-8] were analysed. All parameters were within normal values and similar to the controls the first hours after stroke. Terminal complement complex (TCC) increased significantly from 0·54 to 0·74 AU/ml at 72 h (P = 0·032), reached maximum at 7 days (0·90 AU/ml, P  & lt; 0·001), was still significantly increased at 12 days (0·70 AU/ml, P = 0·009) and thereafter normalized. CRP increased significantly from 1·02 to 2·11 mg/l at 24 h (P = 0·023), remained significantly increased for 1 week (2·53–2·94 mg/l, P = 0·012–0·017) and thereafter normalized. TCC and C-reactive protein (CRP) correlated significantly (r = 0·36, P  & lt; 0·001). The increase in TCC and CRP correlated to the size of infarction (r = 0·80 and P = 0·017 for TCC; r = 0·72 and P = 0·043 for CRP). No significant changes were seen for adhesion molecules and cytokines. In conclusion, transitory systemic complement activation takes place after stroke. The early rise in CRP and the following TCC increase suggest a possible role for CRP in complement activation, which may contribute to inflammation after stroke.
    Type of Medium: Online Resource
    ISSN: 0009-9104 , 1365-2249
    URL: Article
    DOI: 10.1111/j.1365-2249.2004.02489.x
    RVK:
    XA 36770
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2004
    detail.hit.zdb_id: 2020024-9
    Location Call Number Limitation Availability
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Antibodies to CRMP3–4 associated with limbic encephalitis and thymoma
    Oxford University Press (OUP) ; 2007
    In:  Clinical and Experimental Immunology Vol. 149, No. 1 ( 2007-04-25), p. 16-22
    Details
    In: Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 149, No. 1 ( 2007-04-25), p. 16-22
    Abstract: We present a case with subacute limbic encephalitis (LE) and thymoma. Neither classical onconeural antibodies nor antibodies to voltage gated potassium channels (VGKC) were detected, but the serum was positive for anti-glutamic acid decarboxylase (GAD). The patient serum also stained synaptic boutons of pyramidal cells and nuclei of granule cells of rat hippocampus. The objective of the study was to identify new antibodies associated with LE. Screening a cDNA expression library identified collapsin response mediator protein 3 (CRMP3), a protein involved in neurite outgrowth. The serum also reacted with both CRMP3 and CRMP4 by Western blot. Similar binding pattern of hippocampal granule cells was obtained with the patient serum and rabbit anti-serum against CRMP1–4. The CRMP1–4 antibodies stained neuronal nuclei of a biopsy from the patient's temporal lobe, but CRMP1–4 expression in thymoma could only be detected by immunoblotting. Absorption studies with recombinant GAD failed to abolish the staining of the hippocampal granule cells. Our findings illustrate that CRMP3–4 antibodies can be associated with LE and thymoma. This has previously been associated with CRMP5.
    Type of Medium: Online Resource
    ISSN: 0009-9104 , 1365-2249
    URL: Article
    DOI: 10.1111/j.1365-2249.2007.03379.x
    RVK:
    XA 36770
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2007
    detail.hit.zdb_id: 2020024-9
    Location Call Number Limitation Availability
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    Online Resource
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