Mimotopic peptide immunotherapy for the treatment of multiple sclerosis, an inflammatory autoimmune disease.

Several lines of evidence suggest that mast cells play a key role in the pathogenesis of Multiple Sclerosis (MS). The contribution of mast cells likely depends upon specific adherence to myelin surface-bound IgE, which triggers degranulation and the release of enzymes that damage central nervous system (CNS) neurons. To block mast cell degranulation, a peptide-based system was developed to neutralize endogenous, myelin-targeting autoantibodies, thus halting the pathological autoimmune process.

Interplaying factors that effect multiple sclerosis causation and sustenance.

The author hypothesized that multiple sclerosis (MS) is a humoral autoimmune disease, caused by faulty interplay between myelin-specific, dimeric IgE, specifically competing non-IgE antibodies and IgE-triggered degranulating mast cells. The principal fault was believed to be insufficient quantity of protective, specific non-IgE antibodies. Also conjectured was the possibility of an unexpected and adverse immune suppression caused by none-MS pharmaceuticals being consumed by patients for their MS or for other conditions.

Serum IgE reactive against small myelin protein-derived peptides is increased in multiple sclerosis patients.

Though independent findings suggest roles for the allergic arm of the immune system and myelin-reactive antibodies in MS, myelin-reactive IgE has not been investigated. We have developed a radioimmunoassay that measures reactive IgE, IgG and IgA against short (5-6-mers) myelin protein-derived peptides bearing little to no sequence identity with other human proteins, and which might therefore be targets of a CNS-specific autoimmune attack. Here we show that, irrespective of clinical subtype, MS patients' sera are characterized by a higher frequency of measurable IgE against the peptides.

The role of allergy in manifestations of respiratory disease in adult cystic fibrosis.

Background: Variability is present in the expression of the clinical phenotype in cystic fibrosis (CF). Part of this variability may be explained by the coexistence of allergy in CF.

Objective: To determine the rate of allergy in adult CF and evaluate the association between allergy and the manifestations of upper and lower airway disease.