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Eighteen sera containing cold hemagglutinins were examined. IgM levels were determined before and after absorption of this cold antibody. In 5 sera with M-components (immunologic type M kappa) 33 per cent, 93 per cent, 93 per cent, 95 per cent, and 75 per cent of the total IgM was serologically active—that is, lost after the absorption. In 12 sera with no M-component (polyclonal), 0-24 per cent of the IgM molecules had cold activity. One exception was noted in a serum from a patient with cold agglutinin disease containing no monoclonal M-component, but which lost 66 per cent of its IgM after absorption with stromata. No correlation existed between cold agglutinin titer, total IgM-concentration, or per cent active IgM molecules. The results indicate a general qualitative difference between polyclonal and monoclonal cold hemagglutinins.

1. Five patients with congenital or acquired agammaglobulinemia, lacking detectable IgA in serum or saliva, were transfused with 1 to 2 liters of normal plasma. In 2 of these patients IgA was demonstrated in parotid saliva collected after transfusion, but in none of the 5 was salivary IgG or IgM found. This observation indicates the selective transport of IgA into saliva. 2. The observation by others of an immunochemical difference between serum and sahvary IgA globulin was confirmed. In contrast to serum IgA, salivary IgA is attached to a protein having antigenicity which migrates as a gamma1 globulin. We have termed this protein component "transport piece". 3. The transport piece has been found in an unbound form in the saliva of persons completely lacking IgA: agammaglobulinemic patients, ataxia-telangiectasia patients, a healthy person lacking IgA, and a newborn infant. Free transport piece still occurs in the normal child's saliva after IgA production begins. By adulthood there is usually no free transport piece in the saliva. 4. Heat-aggregated salivary IgA, like heat-aggregated serum IgA, does not fix complement. 5. Our findings offer support for the view that there is a distinct local antibody system for the protection of the mucous surfaces.

Aleutian disease (AD) is characterized in mink by marked hypergammaglobulinemia; plasma-cell infiltration of liver, kidneys, and lymph nodes; and terminal bleeding tendency. A survey of fur-farm associates was prompted by a report of a fatal illness, similar in some clinical and pathological aspects to AD, in a mink rancher. Particular attention was directed toward quantitative measurement of immunoglobulins IgG, IgA, and IgM as an index of possible subclinical AD infection. No distinct immunoglobulin abnormalities among the fur-farm associates were uncovered when compared to controls matched for age and sex. Since the presumed infectious agent has not yet been isolated or characterized, direct serologic testing for specific AD antibody among mink handlers cannot yet be evaluated.