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H H Fudenberg

Publications and source records attributed to H H Fudenberg.

At least 397 records · Page 22Linked to original sources
PubMed1972

Experimental allergic encephalitis. Dissociation of cellular immunity to brain protein and disease production.

The encephalitogenic determinant of brain protein, a nonapeptide having the amino acid sequence Phe-Ser-Trp-Gly-Ala-Glu-Gly-Gln-Lys, has been characterized and synthesized. In a previous study, analogues of this encephalitogenic peptide were synthesized and some were shown to be encephalitogenic while others were not. Guinea pigs were immunized with encephalitogenic peptides having amino acid sequences different from that in the native protein. These guinea pigs did not show cellular immunity in vivo (skin reactivity) or in vitro (lymphocyte stimulation or macrophage migration inhibition) to the encephalitogenic brain protein (EP) although they did show cellular immunity to the immunizing antigenic peptide. Guinea pigs immunized with an encephalitogenic peptide having the same amino acid sequence as the brain protein, or with a nonencephalitogenic peptide having the same amino acid sequence as the native protein but lacking the terminal lysine, did develop cellular immunity to the EP. Animals immunized with EP showed cellular immunity to this protein, but not to the encephalitogenic peptides. Animals immunized with nonencephalitogenic protein (NEP), prepared by altering the tryptophan residue of EP, did not develop disease but did show cellular immunity in vitro and in vivo to the EP. Animals protected from disease by immunization with NEP similarly showed cellular immunity to EP. Thus, the results suggest a dissociation between cellular immunity to EP and the production of experimental allergic encephalitis (EAE). Animals immunized with the encephalitogenic peptides develop EAE, but do not show cellular immunity to EP, and animals immunized with NEP show cellular immunity to EP but do not develop EAE. A fresh approach to the examination of the pathogenesis of EAE is now possible through the use of these well-characterized antigens.

Amino Acid Sequence↗
PubMed1972

Development of cellular immunity in the human fetus: dichotomy of proliferative and cytotoxic responses of lymphoid cells to phytohemagglutinin.

The reactivity of cells in vitro was investigated with specimens from various lymphoid organs of seven human fetuses. Thymocytes responded to stimulation by phytohemagglutinin with significant increases in synthesis of DNA, but failed to produce destruction of xenogeneic target cells. In cells from bone marrow, precisely the converse pattern of reactivity to the mitogen was detected. Lymphocytes from spleen and peripheral blood demonstrated both phytohemagglutinin-dependent functions, while hepatic cells did not respond to phytohemagglutinin. Based on the striking dichotomy of phytohemagglutinin-dependent responses in fetal thymocytes and bone-marrow lymphoid cells, we conclude that phytohemagglutinin-dependent cytotoxicity and DNA synthesis are functions of different populations of lymphoid cells during human embryonic development.

Animals↗
PubMed1972

Quantitative abnormalities of allotypic genes in families with primary immune deficiencies.

Genetic antigens of human immunoglobulin G (Gm factors) were measured in members of the families of selected patients with primary immunodeficiency. The sera of seven out of 27 heterozygous relatives had either deficient concentrations of one Gm allotype or an unbalanced ratio of Gm(f)/Gm(a). Since these markers for allelic IgG1 genes are found in almost equal amounts in normal heterozygous persons, the results suggested that there was a quantitative deficiency in the expression in serum of one Gm gene. In several families allotype abnormalities were found in three successive generations; in one instance the quantitative defect appeared to segregate independently of the Gm genes. The experimental data failed to support a recessive gene hypothesis, in that too few of the close relatives had evidence indicating that they were carriers of defective Gm genes. The results were interpreted as consistent with an inherited regulatory defect in certain families with this disorder.

Adolescent↗
PubMed1972

The human rosette-forming cell as a marker of a population of thymus-derived cells.

Sheep red blood cells can surround, in vitro, some human peripheral blood lymphocytes in a formation called a rosette. The number of rosetteforming cells (RFC) in 50 normal persons had a wide range (4-40%). The organs of 13 human fetuses (11-19 wk conceptional age) were examined for the presence of RFC. The thymus possessed the highest percentage of RFC, the maximum being 65% of total thymocytes in two 15-16 wk fetal specimens. Blood RFC were always present and their number slightly increased in the oldest fetuses. The bone-marrow showed 0-8% in the six fetuses studied. RFC were found in the spleen around the 13th wk and in the liver around the 17th wk of gestation. These observations lead to the hypothesis that human blood RFC may be chiefly thymic derived. Studies of patients with immunological disorders support this hypothesis: one patient with Nezelof syndrome had no blood RFC and four patients with Wiskott-Aldrich syndrome had a low number of blood RFC (1 and 1.5%). Patients with acquired hypogammaglobulinemia showed a normal percentage of RFC. With the fetal thymocytes, the percentage of inhibition with anti-mu serum increased with the fetal age to become complete in the oldest fetuses studied. Incubation of the oldest fetal thymocytes or the blood lymphocytes with anti-gamma serum of anti-mu serum completely inhibited the rosette formation. These results suggest that mu-chain determinants are present on human fetal thymocytes and blood RFC. The significance of the presence of gamma-chain determinants on these cells is unclear.

Adolescent↗
PubMed1972

The Wiskott-Aldrich syndrome. Results of transfer factor therapy.

12 patients with Wiskott-Aldrich syndrome were treated with therapeutic doses of transfer factor in an attempt to induce cellular immunity. Clinical improvement was noted after transfer factor therapy in 7 of the 12 patients treated. Because this disease has a variable course and temporary spontaneous improvement can occur, the observed improvement cannot necessarily be attributed to the transfer factor. However, in two patients repeated remissions consistently followed transfer factor administration on repeated occasions. This included freedom from infections, regression of splenomegaly, and clearing of eczema. An unexpected finding was a decrease in bleeding in 3 of the 10 patients who had bleeding. Conversion of skin reactivity was obtained in all seven patients who clinically seemed to respond to transfer factor. In vitro studies performed after the administration of transfer factor demonstrated that the lymphocytes of the patients now produced migration inhibitory factor in response to appropriate test antigens, but did not undergo increased radioactive thymidine incorporation in response to the same antigens. A defect in the monocyte IgG receptors has been found in certain patients with the disease, and the current study shows that all patients with defective monocyte IgG receptors responded to transfer factor, whereas only one patient with normal receptors showed any response. This test may thus prove to be useful in predicting the results of transfer factor therapy in patients with Wiskott-Aldrich syndrome, although evaluation of a larger series of patients will be necessary to confirm this point. We conclude that cellular immunity can be induced, that there appears to be clinical benefit in certain patients with Wiskott-Aldrich syndrome by the use of transfer factor, and that this mode of therapy warrents trial in these patients and others with defects of cellular immunity.

Cell Migration Inhibition↗