Measurements of fecal MPO, EPX and IL-1beta could be objective complements to endoscopical and histopathological evaluations in the daily care of patients with UC.
Increased levels of EPX, MPO and tryptase were observed in stools from collagenous colitis patients, whereas the levels in IBS patients did not differ from healthy controls. Our data suggest that faecal markers could be used as part of the clinical work-up to determine which patients should be biopsied and evaluated for collagenous colitis.
Lupus disease is marked by B lymphocyte hyperactivity and the production of Abs to dsDNA. The production of these anti-dsDNA Abs is T lymphocyte dependent. However, it is not clear how CD4+ T lymphocytes provide help for B lymphocytes to produce IgG anti-dsDNA Abs. One possible mechanism is suggested by studies showing that human patients with systemic lupus erythematosus and lupus mice have increased numbers of CD40 ligand (CD40L)+ T and B lymphocytes. The results described in this study reveal that young, clinically healthy lupus-prone New Zealand Black × New Zealand White F1 (BWF1) mice have naive CD4+ T cells with preformed CD40L. These cells contribute to a brisk response to immunization and to the production of anti-dsDNA Abs. In vitro experiments revealed that CD4+ T cells with preformed CD40L could, upon stimulation, provide antiapoptotic signals for B cells but could not induce proliferation or reduce activation threshold. These results suggest that the direct target cells for the effect of T cells with preformed CD40L in lupus may not be B lymphocytes.
Our previous studies have demonstrated that injection of rheumatoid arthritis (RA) synovial fluid (SF) induces a marked increase mainly of IgG1 antibody-producing cells in autoimmune disease prone (NZB x NZW)F1 mice but not in CBA mice. In the present study, the in vivo effect of RA-SF on autoantibody production was tested in different strains of mice. Injection of RA-SF induced the production of unorthodox autoantibodies (IgG1 rheumatoid factor, RF) in young (NZB x NZW)F1 mice as well as in their parental strains NZB and NZW, but not in normal mice (CBA) or in mice with severe combined immunodeficiency, indicating that the response is not caused by a conventional immune response against RA-SF material. IgG1 RF production was rapidly induced and reached high levels already on day 7 and lasted for more than 90 days. The induction of IgG1 RF was not the result of polyclonal activation, since RA-SF did not stimulate the production of other antibodies, such as autoantibodies against double-stranded DNA, bromelain-treated mouse red blood cells, myosin, transferrin, cytochrome c, thyroglobulin or myoglobin or antibodies reactive with the hapten TNP. To elucidate the identity of the active substance in RA-SF, responsible for IgG1 RF production, bound and unbound material of RA-SF, eluted from a protein-G column was injected into (NZB x NZW)F1 mice. Only the protein-G binding material was active, indicating that the effect is mediated by autoantibodies or immune complexes in the synovial fluid. Further studies demonstrated that identical concentrations of protein obtained from a pool of normal human IgG or SF from seronegative RA and non-RA arthritides patients did not contain the same activity.
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