PubMed · 4114514
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1972-08-05. What makes bacteria pathogenic?. https://pubmed.ncbi.nlm.nih.gov/4114514/
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The fate of the neutralizing antibody (NAB) in MS patients treated with interferons remains unclear. We conducted a follow-up survey of NAB titers in 59 long-term treated patients from the London and Vancouver cohorts of the pivotal trial of interferon alpha-1b. NAB were measured with the myxovirus protein A assay and an ELISA, at a mean follow-up that exceeded 8 years. NAB disappeared in the majority of patients.
The authors review the clinical signs of the five most frequent allergic diseases of the conjunctiva (seasonal allergic conjunctivitis, perennial allergic conjunctivitis, vernal conjunctivitis, atopic conjunctivitis and giant papillary conjunctivitis), and then the immunologic bases of the development of the early-type allergic reaction. In the course of this, they describe the roles played by IgE globulin and the mastocytes in histamine release, and also the possible effects manifested in allergic inflammation in consequence of the metabolic products of arachidonic acid formed in the cell membrane (leukotrienes, lipoxins, prostaglandins and thromboxanes). Following this, they present an account of the process by which the eosinophilic cells that play the main role in the later stages of allergic inflammation emerge from te vascular bed, and the effects of various adhesion molecules. Finally, they discuss a new classification of conjunctivitis (proposed by Bonini), based on the pathomechanisms of the diseases.
BACKGROUND: Autoantibodies against synthetic peptides of beta-adrenergic receptors have been observed in human cardiomyopathy. However, it has never been shown that such antibodies really interact with native human beta-adrenergic receptors, nor has the clinical impact of such an interaction been investigated in larger groups of patients. METHODS AND RESULTS: We screened 104 patients with dilated or ischemic cardiomyopathy (NYHA functional classes II to IV) and 108 healthy subjects for IgG antibodies reacting with beta-receptor peptides. Such IgGs were further analyzed for binding and functional interactions with native recombinant human beta-adrenergic receptors. Antibodies reacting with synthetic receptor peptides were present in 51% of the patients. However, only a subgroup directed against the second extracellular receptor domain also recognized native human beta-adrenergic receptors situated in a cell membrane. All antibodies of this subgroup impaired receptor ligand binding and enhanced receptor-mediated signaling, which could be blocked by 5 micromol/L bisoprolol in vitro. Their prevalence was 1% in healthy subjects and 10% in ischemic cardiomyopathy, whereas it amounted to 26% in dilated cardiomyopathy and was associated with a significantly poorer left ventricular function. CONCLUSIONS: Our data show that activating autoantibodies against human beta-adrenergic receptors exist in approximately 25% of patients with dilated cardiomyopathy. Counteraction of such autoantibodies might contribute to the beneficial effects of beta-adrenergic receptor blockade in chronic heart failure.