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J D Feldman

Publications and source records attributed to J D Feldman.

At least 109 records · Page 6Linked to original sources
PubMed1969

Heterogeneity of antibody-forming cells. An electron microscopic analysis.

Cell suspensions from draining lymph nodes of immune and nonimmune rats were reacted in vitro with (125)I-labeled antigens. In light microscopic radioautographs of smears, 17% of the immunized cells were tagged by specific antigen; 2.0% of control cells were positive. In electron microscopic radioautographs, 90% of the labeled elements from immune donors were lymphocytes, blast and plasma cells; 10% were monocytes-macrophages or other elements, including naked nuclei. 15% of the labeled cells from control materials were lymphocytes and plasma cells, while 85% were monocytes-macrophages and naked nuclei. Within cell suspensions derived from immunized animals there were almost twice as many lymphocytes marked by isotope as plasma cells, and the lymphocytes ranged in morphology from mature monoribosomal elements to immature polyribosomal cells. Antibody-forming cells fixed labeled antigen at their surfaces. The monocyte-macrophage class was distinguished by a high mean grain count and by distribution of grains within cytoplasmic vacuoles and lysosomes.

Animals↗
PubMed1969

Graft rejection.

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Antigen-Antibody Reactions↗
PubMed1968

Cytology of immunologic memory. A morphologic study of lymphoid cells during the anamnestic response.

Pairs of rats were immunized with keyhole limpet hemocyanin (KLH) and simultaneously labeled with thymidine-methyl-(3)H or 5-iodo-2'-deoxyuridine-(125)I. From 10-50 days later, their lymphoid organs were examined 3 days after anamnestic stimulation with KLH or after primary injection of BGG. Light and electron microscopic study of the labeled cells revealed that immunologic memory resided in the mature resting monoribosomal lymphocyte which, upon stimulation, transformed to an immature polyribosomal lymphocyte and mitotically active blast cell. These latter elements differentiated into plasma cells directly or after mitosis.

Animals↗
PubMed1967

Renal homotransplantation in rats. I. Allogeneic recipients.

Within 3-6 hr after the reestablishment of the circulation, a characteristic pathology developed in renal homotransplants. Blood monocytes and lymphocytes adhered to large thin-walled vessels of the septa carrying interlobular arteries, traversed their walls, and aggregated in the connective tissue spaces around them. Within 3 days, the number and size of the extravascular cells markedly increased, filling the septa completely and spreading from them centrifugally to occupy the intertubular spaces throughout the cortex. The composition of these aggregates at first was a mixture of lymphocytes and monocytes, and later consisted of large blast cells, macrophages, a few plasma cells, and polymorphonuclear leukocytes. Mitotic activity was seen 2 days after surgery among the large blast cells and increased to a maximal level a day later. Coevally with these changes, the thin-walled septal vessels, intertubular veins and capillaries, and finally, arteries and arterioles, in that order, were damaged. Focal injury of tubules was slight 24 hr after homografting; widespread cortical necrosis had developed 5-7 days later. At no time up to 7 days were concentrations of immunoglobulins detected by fluorescence microscopy in the transplanted kidneys. The morphologic manifestations and temporal sequences of renal homograft destruction suggested that several mechanisms acted synergistically to eliminate the transplant. The initial injury appeared to be the result of an interaction between host lymphoid cells and target endothelium, a phenomenon akin to allogeneic inhibition; followed by spreading ischemia; additional contact injury to tubules; and nonspecific inflammation associated with necrobiotic tissue.

Animals↗
PubMed1967

Autoradiographic plaques for the detection of antibody formation to soluble proteins by single cells.

Single cells that synthesize antibody to soluble proteins can be detected and counted by an autoradiographic procedure. The method is based on the specific binding of I(131)-labeled antigen to the antidogy which has been produced by and has diffused around cells in an agarose medium and which has been precipitated by an antibody to gamma globulin. The antigen-binding zones appear as dark spots on high-speed x-ray film exposed to the dried agarose preparations.

Animals↗