A method is described for the adsorption of selected macromolecules to colloidal gold which is then used as an electron dense marker for the indirect detection of specific cell surface molecules. Membrane bound concanavalin A, which binds specific sugars on horseradish peroxidase, and wheat germ agglutinin, which binds specific sugars on ovomucoid are detected indirectly with gold labeled horseradish peroxidase and ovomucoid, respectively. Goat anti-human IgM on blood lymphocytes is detected with gold labeled rabbit anti-goat IgG. In the preparation of colloidal gold labeled proteins, the problems of flocculation of colloidal gold by proteins and nonadsorption of proteins to colloidal gold, are solved through a combination of concentration of protein and pH variable adsorption isotherms, which allows one to determine the conditions for adsorption of proteins to colloidal gold. Adsorption is pH dependent, the pH conditions correlating with the isoelectric point(s) of the major protein fraction(s); adsorption is influenced by interfacial tension, solubility and by the electrical charge on the molecules. Colloidal gold is inexpensive and preparation of a useful label is rapid, reproducible and the results easily quantitated from electron micrographs.

Adsorption of horseradish peroxidase, ovomucoid and anti-immunoglobulin to colloidal gold for the indirect detection of concanavalin A, wheat germ agglutinin and goat anti-human immunoglobulin G on cell surfaces at the electron microscopic level: a new method, theory and application.

https://www.amjmed.com/article/0002-9343(75)90606-3/pdf

Drug-induced immune hemolytic anemia

Rheumatoid factor: Its nature, specificity, and production in rheumatoid arthritis

Deficiency of immune interferon production by leukocytes of normal newborns

Burnet has postulated that autoimmunity arises from emergence of “forbidden clones” which make auto-antibody. Our postulate, in contradistinction, is that auto-antibody-producing cells are always present, producing enough autoantibody to remove damaged or aged tissues. In normals, the number of such cells is kept in check by normal T-cells. When T-cell function is defective, the “governing system” controlling auto-antibody producing clones fails, and autoimmune disease, mediated in most diseases by cellular immunity, emerges. The governing mechanism in normals may be one analogous to that which limits the amount of antibody produced to a given antigen, and keeps the antibody (and Ig levels) from continuously rising in normal subjects. Experimental data for this concept are provided by several lines of evidence: 1) Normals have low levels of rheumatoid factor and other “auto-antibodies” in their serum.

https://www.amjmed.com/article/0002-9343(71)90263-4/pdf

Genetically Determined Immune Deficiency As the Predisposing Cause of “Auto-Immunity” and Lymphoid Neoplasia

https://www.amjmed.com/article/S0002-9343(70)80123-1/pdf

Insulin Resistance in Juvenile Diabetes Mellitus Immunologic Studies

Morphology and nucleoside incorporation of human neonatal lymphocytes.

The use of chromic chloride as a coupling reagent has made it possible to coat red cells with rhinovirus protein. This is shown by immunofluorescence, electron microscopy and immunocolloidal experiments.

Passive Haemagglutination Test for Anti-rhinovirus Antibodies

https://www.amjmed.com/article/0002-9343(74)90621-4/pdf

W. Page Faulk

Papers

Insulin Resistance in Juvenile Diabetes Mellitus Immunologic Studies

Morphology and nucleoside incorporation of human neonatal lymphocytes.

Passive Haemagglutination Test for Anti-rhinovirus Antibodies

Maternal antibody to fetal light chain (Inv) antigens

Nutrition and immunity