Albert H. Coons
Harvard University
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Featured researches published by Albert H. Coons.
Experimental Biology and Medicine | 1941
Albert H. Coons; Hugh J. Creech; R. Norman Jones
Summary A β-anthryl-carbamido derivative of antipneumococcus III rabbit antibody retains the original immunological properties while rendering Type III pneumococci specifically fluorescent in ultraviolet light. It is a pleasure to acknowledge the constant advice and help so generously given by Dr. John F. Enders and Dr. Allan L. Grafflin, and the kind interest shown by Dr. Louis F. Fieser.
Experimental Biology and Medicine | 1954
Thomas H. Weller; Albert H. Coons
Summary Tissue culture preparations infected with agents originally derived from the eruptive lesions of cases of varicella and herpes zoster, as well as control preparations infected with the virus of herpes simplex, were studied by a modification of the fluorescent antibody technic. Employing the infected preparations as antigen, fixation of antibody from human sera derived from cases of varicella, herpes zoster or herpes simplex was detected by the use of a fluorescent antihuman gamma globulin conjugate. Antibody reacting with the varicella and herpes zoster antigens to an almost identical degree appeared during convalescence in serum specimens derived either from cases of varicella or from cases of herpes zoster. Antibody reacting with herpes simplex virus was demonstrated uniformly only in a group of sera derived from cases of recurrent herpes simplex. Immunologic evidence was thus obtained to support the thesis that the etiologic agents of varicella and herpes zoster have been isolated and propagated in vitro.
International Review of Cytology-a Survey of Cell Biology | 1956
Albert H. Coons
Publisher Summary The use of specific antibody as a histochemical reagent depends on the fact that dye molecules can be chemically linked to antibody molecules without impairing the capacity of the antibody to react specifically with the substance (antigen), which stimulated its synthesis. The specific step in an immune reaction is the deposit from a solution of labeled antibody molecules over those areas of tissues and cells where the antigen is present; unreacted antibody and inert labeled proteins remain in solution and can be washed away leaving on the slide a labeled protein deposit, which can be seen under the microscope. The use of labeled antibody requires a certain familiarity with the methods and tradition of immunology, as well as with the more strictly practical procedures used in the purification of antigens and the production of antisera.
Experimental Biology and Medicine | 1962
Howard S. Rubenstein; Jacob Fine; Albert H. Coons
Summary and conclusion A minimal lethal dose of E. coli 0111:B4 endotoxin was injected intravenously into 3 dogs. Two were killed, one 10 and one 90 minutes after endotoxin administration. The third died of endotoxemia in 13 hours. By immunofluorescence, endotoxin was found in patchy distribution throughout the walls of the peripheral vascular system: frequently in the endothelium of capillaries and venules and, extra-cellular as well as intracellular, in the walls of veins; and, on occasion, extracellular and intracellular, in the media of arterioles and muscular arteries. Endotoxin was also detected in polymorphonuclear leukocytes, both free in the peripheral circulation and in unusual tissue sites; for example, within vessel walls and aggregated in the sinuses of the liver. Particles of endotoxin were frequently seen free in the lumens of blood vessels; in some instances endotoxin appeared to be fixed to the intima of vessels; and masses of endotoxin occasionally completely filled a vascular lumen, most often in renal glomerular capillaries, in the adrenal medullary sinuses, and in liver sinues. Endotoxin was widely distributed throughout the reticulo-endothelial system, including histiocytes. Qualitatively and quantitatively, the distribution of endotoxin within the 3 dogs was similar. We infer from the presence of endotoxin in blood vessel walls that endotoxin may be acting directly upon these structures to produce the peripheral vascular collapse of lethal endotoxemia.
Science | 1970
Farrokh Modabber; Shigeru Morikawa; Albert H. Coons
The thymus of a normal adult mouse contains lymphocytic cells with a large number of antigen-binding receptors. Binding of the antigen by these cells is specific and can be inhibited by cross-reactive materials. It is possible that the interaction of thymocytes with antibody-forming precursor cells, required in the primary immune response to certain antigens, is mediated by these specific antigen-binding cells of the thymus.
Experimental Biology and Medicine | 1951
Tien-Hsiuo Chu; F. S. Cheever; Albert H. Coons; Joan B. Daniels
Summary The distribution of mumps virus in one experimentally infected monkey 96 hours after inoculation has been investigated by simultaneous labelled antibody and virus isolation studies. The results furnished by the two methods were in fair agreement. Virus was demonstrated in CNS (brain and spinal cord) as well as in both parotid glands, although the animal had shown no neurological signs. No virus was demonstrated in the other organs examined.
Experimental Biology and Medicine | 1976
Shigeru Morikawa; Albert H. Coons
Summary Enumeration of the cells in the mouse spleen making a specific response to antigenic stimulation indicates that the first detectable antibody appears in a few cells in the red pulp in the first 12 hr; later, such cells appear in the white pulp, and, though their number increases in both locations, the gain is more rapid in the white pulp, reaching a peak on the 12th day in the primary response, and on the 5th in the secondary, when there are two to four times as many cells there as in the red pulp. The response in the white pulp requires a higher threshold dose than that in the red pulp. We thank Inez Serur and Nancy Delancy for devoted technical help during the performance of these experiments.
Archive | 1969
Geronimo Terres; Albert H. Coons
An enhancing influence of preexisting antibody on the magnitude of antibody response to an antigenic stimulus was first noted by Terres and Wolins [1]. Despite the general finding by many workers that passively administered antibody inhibits antibody formation (reviewed by Uhr and Moller [2]), the original observation has been repeatedly confirmed by the senior author and his colleagues (e.g., [3, 4]). The difference evidently is in the dosage and in the need for antigen excess or for the presence of antigen on two occasions, as suggested by Leduc et al. [5]. The kinetics and the quantity of antibody synthesized in such an enhanced response were indistinguishable from those of a secondary response (S. L. Morrison and G. Terres, unpublished); mouse anti-BSA appeared within 5 days of the booster or the antigen-antibody injection, and the peak titer was reached on about day 7.
Journal of Experimental Medicine | 1949
Albert H. Coons; Melvin H. Kaplan
Journal of Experimental Medicine | 1955
Albert H. Coons; Elizabeth H. Leduc; Jeanne M. Connolly