SUMMARYIn this study we demonstrate that IgG present in the sera of patients with primary Sjögren's syndrome (PSS) could bind and activate muscarinic acetylcholine receptors (mAChRs) of rat parotid gland. These antibodies were able to inhibit in a non-competitive manner the binding of 3 H-quinuclidinyl benzilate (QNB) to mAChRs of purified rat parotid gland membranes. Moreover, IgG from PSS could modify biological effects mediated by mAChR activation; i.e. decrease cAMP, increase phosphoinositide turnover without affecting cGMP. Atropine and 4-DAMP blocked all of these effects, and carbachol mimicked them, confirming the M 3 subtype mAChRs mediated PSS IgG action. Neither binding nor biological effect were obtained with IgG from sera of normal women. The prevalence of cholinergic antibody was 100% in PSS, and was independent of Ro/SS-A and La/SS-B antibodies. It could be concluded that antibody against mAChRs may be another serum factor to be considered in the pathophysiology of the development of PSS.

Abstract. The relative reactivities with native and denatured DNA of 35 lupus sera were investigated by quantitative complement fixation and precipitin studies and showed great variations. The use of purified native DNA demonstrated that, in at least 22 of these 35 sera, the anti-DNA antibodies reacted with the native form, independently of denatured contaminants. Systemic lupus sera were shown to contain three main types of DNA antibodies: those reacting only with denatured DNA, those reacting to the same extent with both forms of DNA, and those reacting preferentially with native DNA. In some instances, the latter antibodies fix complement and precipitate only with native DNA but are inhibited by the denatured form. This finding points to the importance of conformation in the antigenic structure of DNA. The simultaneous occurrence of different varieties of DNA antibodies was demonstrated in several sera. Evidence was obtained that some of these human antibodies to DNA can belong to the IgM class. Thus, DNA antibodies from systemic lupus patients differ in many respects from most of the experimentally produced antibodies capable of reacting with DNA.

Ultrastructural and immunohistochemical studies on tissues from five patients with Argentine hemorrhagic fever revealed previously undetected lesions caused by the viral infection. Two types of particle were seen in the cells of all organs examined. The particles had some characteristics similar to those described for arenaviruses. However, the virus-like particles were intracellular, had a single membrane, and apparently originated by a process of budding into the endoplasmic reticulum cisternae. Intranuclear bodies and three types of cytopolasmic change were observed in conjunction with the virus-like particles; Antigenic determinants of Junin virus were demonstrated in cells of all organs examined. Immunohistochemical experiments also indicated alterations in the cellular mechanisms of protein synthesis. Until now the pathogenesis of human diseases produced by arenaviruses has not been established. The results of this study suggest that in Argentine hemorrhagic fever the virus is responsible for a direct pathogenic action.