[Skin tests for general anesthetics]. / Tests cutanés aux anesthésiques généraux.

During a meeting between anaesthetists and allergists, skin tests were presented to show their value and the difficulties to which they give rise when they are weak. General principles, techniques and readings are described first. As usual, it is sensitivity, specificity and negative predictive value that are at the centre of attention. Selected clinical cases are given as examples. The high prevalence of cases who show a latent sensitisation to curare indicates an increase in allergological tests to patients who present risk factors.

Mimicry between receptors and antibodies. Identification of snake toxin determinants recognized by the acetylcholine receptor and an acetylcholine receptor-mimicking monoclonal antibody.

In several instances, a monoclonal antibody raised against a receptor ligand has been claimed to mimic the ligand receptor. Thus, a specific monoclonal antibody (Malpha2-3) raised against a short-chain toxin from snake was proposed to mimic the nicotinic acetylcholine receptor (AChR) (). Further confirming this mimicry, we show that (i) like AChR, Malpha2-3 elicits anti-AChR antibodies, which in turn elicit anti-toxin antibodies; and (ii) the region 106-122 of the alpha-chain of AChR shares 66% primary structure identity with complementarity-determining regions of Malpha2-3. Also, a mutational analysis of erabutoxin a reveals that the epitope recognized by Malpha2-3 consists of 10 residues, distributed within the three toxin loops. Eight of these residues also belong to the 10-residue epitope recognized by AChR, a result that offers an explanation as to the functional similarities between the receptor and the antibody. Strikingly, however, most of the residues common to the two epitopes contribute differentially to the energetic formation of the antibody-toxin and the receptor-toxin complexes. Together, the data suggest that the mimicry between AChR and Malpha2-3 is partial only.

CD and FTIR studies of an immunogenic disulphide cyclized octadecapeptide, a fragment of a snake curaremimetic toxin.

In a previous paper, the systematic epitope screening of a snake curaremimetic toxin or toxin a was described by this group using a panel of synthetic octadecapeptides. The disulphide cyclized peptide (Cys-23,40)(23-40) corresponding to loop II of the native toxin was found to elicit, with no linkage to a carrier, neutralizing antisera against the toxin. We have now undertaken the conformational study of this immunogenic disulphide cyclized peptide by CD and FTIR. The CD study of the peptide was carried in aqueous solution under various conditions (pH, temperature, presence of micelles) and in trifluoroethanol solution. Low temperature, SDS micelles and trifluoroethanol were found to induce a beta-sheet formation (16 to 39%). FTIR spectra of the peptide in the solid state (dry film) and in D2O solution or deuterated-TFE solution (hydrated film) displayed some characteristic bands indicating the presence of beta-sheet (1623 cm-1) and beta-turn (1637 cm-1; 1694 cm-1). These studies indicate that the immunogenic disulphide cyclized peptide (23-40) can adopt in solution an ordered structure.

[Clinical correlation of anti-receptor antibody titer, sensitivity to curare and electromyographic changes in experimental autoimmune myasthenia gravis].

Experimental autoimmune myasthenia gravis (EAMG) was studied in 39 rabbits which were repeatedly immunized with purified membrane-bound Torpedo (Nacine timilei) acetylcholine receptor (N-AchR). These rabbits invariably formed anti-AChR antibodies and some of them developed muscular weakness or flaccid paralysis. Pharmacological, physiological and ultrastructural studies showed that the pathological features of EAMG in rabbits closely resembled those of human myasthenia gravis. Antibody titer to AChR of the rabbit sera was determined with ELISA. In some of the rabbits, a rise in antibody Level occurred without appearance of weakness, while it is still likely that AChR antibody could be necessary for the induction of neuromuscular blockage. The sensitivity to curare was found to correlates closely with the severity of the disease. Typical electromyographic changes were found only in some of the EAMG rabbits with these studies. It was considered that anti-AChR concentration would not be the single pathological factor in EAMG.