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Research Article Free access | 10.1172/JCI105625
Rheumatic Disease Unit, Department of Medicine, State University of New York at Buffalo and The Buffalo General Hospital, Buffalo, N. Y.
†Address requests for reprints to Dr. Thomas B. Tomasi, Jr., Dept. of Medicine, State University of New York at Buffalo, 100 High St., Buffalo, N. Y. 14203.
*Submitted for publication February 14, 1967; accepted May 5, 1967.
Supported by U. S. Public Health Service grant AM 10419 and National Science Foundation grant 19-381.
Presented in part at the American Rheumatism Association Meeting in Denver, Colo., June 18, 1966.
Find articles by Stobo, J. in: JCI | PubMed | Google Scholar
Rheumatic Disease Unit, Department of Medicine, State University of New York at Buffalo and The Buffalo General Hospital, Buffalo, N. Y.
†Address requests for reprints to Dr. Thomas B. Tomasi, Jr., Dept. of Medicine, State University of New York at Buffalo, 100 High St., Buffalo, N. Y. 14203.
*Submitted for publication February 14, 1967; accepted May 5, 1967.
Supported by U. S. Public Health Service grant AM 10419 and National Science Foundation grant 19-381.
Presented in part at the American Rheumatism Association Meeting in Denver, Colo., June 18, 1966.
Find articles by Tomasi, T. in: JCI | PubMed | Google Scholar
Published August 1, 1967 - More info
Sucrose density gradient analysis of the fresh sera of patients with hereditary ataxia telangiectasia, disseminated lupus, and Waldenström's macroglobulinemia revealed the presence of an immunoglobulin possessing IgM determinants but having a sedimentation coefficient of approximately 7 S. Bio-Gel chromatography of patients' sera confirmed the presence of two distinct populations of IgM. The low molecular weight IgM possessed incomplete isohemagglutinin activity that was resistant to treatment with reducing agents. Gel diffusion analysis revealed that the 7 S IgM showed immunological identity with both 19 S IgM and the subunits of the 19 S IgM produced by reduction. Approximately 10 to 15% of the patient's total IgM was low molecular weight. Evidence is presented that the 7 S IgM was not produced from the patient's serum 19 S IgM on in vitro incubation. A simple rapid technique is described, using double diffusion in polyacrylamide gels, which permits the determination of low molecular weight IgM in sera and other fluids. Using this technique, the sera of 52 patients with disseminated lupus were surveyed, and 17% of the patients were found to contain low molecular weight IgM. The low molecular weight IgM occurred with particular frequency in male patients with disseminated lupus and in those patients with low or absent serum IgA.
Studies of the salivary immunoglobulins of patients with ataxia telangiectasia and disseminated lupus suggest an iverse relationship between the levels of IgA and IgM. In patients lacking salivary IgA, IgM was the major immunoglobulin present. No correlation was observed between salivary immunoglobulin levels and the severity of sinopulmonary infections in these patients.
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