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- Corthay, Alexandre, et al.
(författare)
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Role of glycopeptide-specific T cells in collagen-induced arthritis: an example how post-translational modification of proteins may be involved in autoimmune disease
- 2001
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Ingår i: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 33:7, s. 456-465
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Tidskriftsartikel (refereegranskat)abstract
- Immunization of mice with type II collagen (CII), a cartilage-restricted protein, leads to collagen-induced arthritis (CIA), a model for rheumatoid arthritis (RA). CIA symptoms consist of an erosive joint inflammation caused by an autoimmune attack, mediated by both T and B lymphocytes. CD4+ alphabeta T cells play a central role in CIA, both by helping B cells to produce anti-CII antibodies, and by interacting with other cells in the joints, eg macrophages. In H-2q mice, most CII-specific CD4+ T cells recognize the CII(256-270) peptide presented on the major histocompatibility complex (MHC) class II Aq molecule. Post-translational modifications (hydroxylation and variable glycosylation) of the lysine residue at position 264 of CII generate at least four different T-cell determinants that are specifically recognized by distinct T-cell subsets. Most T cells recognize CII(256-270) glycosylated with the monosaccharide galactose, which is consequently immunodominant in CIA. Recent studies indicate that the arthritogenic T cells in CIA are glycopeptide-specific, suggesting that induction of self-tolerance may be rendered more difficult by glycosylation of CII. These data open the possibility that outoimmune disease may be caused by the creation of new epitopes by posttranslational modification of proteins under circumstances such as trauma, inflammation or ageing.
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- Johansson, Bertil, et al.
(författare)
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Clinical and biological importance of cytogenetic abnormalities in childhood and adult acute lymphoblastic leukemia
- 2004
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Ingår i: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 36:7, s. 492-503
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Forskningsöversikt (refereegranskat)abstract
- Among the approximately 7,000 cytogenetically abnormal childhood and adult B- and T-lineage acute lymphoblastic leukemias (ALL) published to date, numerous recurring chromosomal aberrations and abnormality patterns have been identified, and it has been clearly shown that the cytogenetic features often correlate closely with specific morphologic, immunophenotypic, and clinical parameters. Thus, karyotypic investigations are now routinely performed for diagnostic and prognostic purposes in ALL, with the chromosomal abnormalities/cytogenetic patterns playing a major role for proper risk assessment and choice of treatment. At the same time, the cytogenetic analyses have resulted in the identification of more than 70 different genes, located at the breakpoints of ALL-associated structural chromosomal abnormalities, that are causally implicated in the leukemogenic process. Hence, the genetic studies have also improved our understanding of the mechanisms of leukemogenesis. However, the almost staggering amount of cytogenetic information presently available has made it increasingly difficult to obtain a general overview of the clinical and biological importance of karyotypic patterns in ALL. Here, we summarize and review the cytogenetic features of childhood and adult ALL, with emphasis on their molecular genetic consequences and their clinical impact.
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- Olsson, Anders, 1940-, et al.
(författare)
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Early initiation of treatment with statins in acute coronary syndromes
- 2002
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Ingår i: Annals of Medicine. - : Informa UK Limited. - 0785-3890 .- 1365-2060. ; 34:1, s. 37-41
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Tidskriftsartikel (refereegranskat)abstract
- Statins may act rapidly to reverse abnormalities of the arterial wall that may predispose to recurrent ischemic events after acute coronary syndromes. Such abnormalities are endothelial dysfunction, a local inflammatory response, and an exaggerated thrombogenic tendency. In one study almost 20 000 patients with first myocardial infarction were studied with regard to statin treatment (28%) or not. Baseline characteristics were adjusted using multivariate regression analysis including propensity analysis. One year mortality was 3.7/5.0% in statin/not statin groups, respectively, P = 0.001, relative risk 0.75. In another study of more than 20 000 patients, 18% were prescribed statin after an acute coronary syndrome and followed for six months. Propensity analysis was performed in this study as well. Deaths in statin/not statin groups were 1.7/3.5%, P < 0.0001, relative risk 0.48. In the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL), a double-blind randomized, placebo-controlled intervention study, 3086 patient with acute non-Q-wave coronary syndromes were allocated immediately in hospital to receive atorvastatin 80 mg daily or placebo for four months. No lower limit for plasma LDL cholesterol was used. Primary endpoint was time to first occurrence of death, non-fatal myocardial infarction, cardiac arrest, and worsening angina with objective evidence of ischemia. This was significantly reduced compared to the placebo group by 2.4% (14.8 versus 17.2%, relative risk 0.84, P = 0.048). Atorvastatin also reduced significantly fatal or non-fatal strokes. Possible mechanisms behind these acute beneficial effects are discussed. The studies highlight the importance of treatment with a statin in the early management of acute coronary syndromes and the need to incorporate this therapeutic strategy in national guidelines and treatment recommendations.
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