[Targeting diagnosis and treatment value of chelating anti-IL-1ß mAb-SPIONs in temporal lobe epilepsy model].

Objective: In order to study the diagnosis and treatment value of chelating anti-IL-1ß mAb-SPIONs in temporal lobe epilepsy model induced by lithium chlorid and pilocarpine. Methods: Forty-five temporal lobe epilepsy model rats were randomly and equally divided into saline group, plain-SPIONs group, anti-IL-1ß mAb-SPIONs group. Each group was injected with equal particles at day 3 and day 14 after the onset of seizures. MRI were conducteds before and 4 hours after particles injection and T2 values were measured. The distribution of iron particles in the epileptic tissue was observed and the neuronal loss, astrocyte proliferation and microglia activation were detected. The expressions of IL-1ß and NF-κBp65 in each group were detected meanwhile. Results: At day 14 after seizure, the value of T2 was 84±14 after injecting anti-IL-1ß mAb-SPIONs. Compared with the control group, the value of T2 obviously declined. These phenomena of neuron loss, astrocyte proliferation and microglia activation had been improved obviously. IL-1ßand NF-κBp65 expression also significantly reduced. Conclusion: Anti-IL-1ß mAb-SPIONs can penetrate blood brain barrier and plays an important role in targeting positioning and targeting therapy in temporal lobe epilepsy.

Inhibition of antigen-specific IgE production by antigen coupled to membrane IgE peptide.

The membrane IgE peptide (MEP) encompassing 20 amino acids proximal to the C terminus of membrane IgE molecules, and secretory IgE peptides (SEP), spanning CH epsilon 1 to 4 domain were synthesized according to IgE genomic and cDNA sequences. Inhibition of anti-KLH and anti-BGG IgE, but not IgG responses was observed in mice treated with MEP-protein but not SEP-protein conjugates in complete/incomplete Freund's adjuvant. Only IgE responses directed toward proteins to which MEP was conjugated, were inhibited, while IgE responses to a concomitantly injected, unrelated antigen were not. Inhibition of antigen-specific IgE was also not correlated with levels of anti-MEP or anti-IgE antibodies, moreover, levels of total IgE remained comparable among mice treated with MEP-protein conjugates, native or glutaraldehyde-modified protein carriers. This observation may have significant import on future design of IgE immunotherapy. Treatment of MEP conjugated allergens prevents formation of IgE-anti-IgE complexes because the MEP sequence is absent from the secretory IgE.