PubMed Health⌕ Search

Biomedical subjects

J D FELDMAN

Publications and source records attributed to J D FELDMAN.

At least 19 recordsLinked to original sources

QUANTITATION OF TRANSPLANTATION IMMUNITY. I. METHOD.

A technique for in vivo quantitation of transplantation immunity has been presented. Known numbers of H(3)-thymidine-labeled lymphoid cells were injected intravenously into isologous or homologous recipients. The total radioactivity in host spleens was counted at different time intervals. The rate of isotope disappearance from the spleen was exponential to 0.5 per cent of the dose or less. In isologous recipients, the calculated half-life of labeled cells was 82 hours; in homologous recipients it was 40 hours; and in presensitized homologous hosts it was 18 hours. The technique is a highly reproducible, precise, and sensitive measure of transplantation immunity.

Animals↗

PASSIVE TRANSFER OF TRANSPLANTATION IMMUNITY. IV. TRANSPLANTATION ANTIBODY FROM EXTRACTS OF SENSITIZED LYMPHOID CELLS.

Passive transfer of homograft immunity was successfully achieved by injection of the supernatant obtained from tissue-sensitized lymphoid cells disrupted by sonic vibration. The effective substance destroyed specific skin homografts within 6 days but did not reject non-specific skin grafts in this time. No evidence of transferred antigen or of transfer factor was found when the effective material was passed to irradiated recipients carrying test grafts. By a variety of physiochemical procedures the "soluble substance" behaved like a gamma globulin and was considered to be a transplantation antibody.

Animals↗

SPECIFICITY OF PASSIVELY TRANSFERRED DELAYED HYPERSENSITIVITY.

Guinea pigs were injected intravenously with lymphoid cells sensitized to tubercle bacilli (TBC cells) and with lymphoid cells sensitized by contact to a simple chemical, dinitrofluorobenzene (DNFB cells). In each transfer, either the TBC cells or the DNFB cells were labeled with H(3)-thymidine. Immediately after transfusion, each recipient was skin tested with PPD and DNFB. 24 hours later these lesions were removed for determination of total radioactivity and for autoradiographic analysis. When TBC cells labeled with H(3)-thymidine were transferred with DNFB cells without an isotopic marker, the total radioactivity and the concentration per gram of skin lesion were greater in the PPD test sites. In the reciprocal arrangement, when DNFB cells labeled with H(3)-thymidine were transfused with TBC cells without an isotopic tag, the total radioactivity and the concentration per gram of skin lesion were greater in the DNFB test site. Similar results were obtained in guinea pigs which were actively immunized by tubercle bacilli and passively by transfer of DNFB cells. Autoradiographic analysis of test sites from guinea pigs passively transferred with both types of sensitized cells confirmed these findings. By calculation, only a very small number of transferred sensitized cells reached the specific test lesion. Most of the cellular infiltrate was derived from the responding host. The specificity of the reaction of delayed hypersensitivity was apparently achieved by retention of the sensitized cells after they had arrived by chance at the specific antigen depot and was not due to a non-specific stickiness of sensitized or inflamed lymphoid cells.

Animals↗

Passive transfer of contact sensitivity by tritiated thymidine-labeled lymphoid cells.

Passive transfer of tritiated thymidine-labeled lymphoid cells sensitized to the simple chemical DNFB into homologous guinea pigs resulted in positive contact skin reactions 24 hours after skin testing with DNFB. Labeled sensitized cells were found to accumulate at these sites, whereas, labeled nonsensitized lymphoid cells did not appear non-specifically in contact skin reaction sites. The labeled cells were small and large lymphocytes and immature cells of the lymphoid series. The maximum reactions were obtained at 24 hours, with an average of 3.4 per cent of the infiltrating mononuclear cells showing a label. At 48 hours, the macro- and microscopic reactions were similar to the 24 hour reactions but diminished in intensity, and the number of labeled cells in the infiltrates had decreased to 1 per cent of the total infiltrating mononuclear cells. (1/4) to (1/3) of the labeled cells were found within the epidermis in the test skin sites. These data have indicated that contact sensitivity, like tuberculin sensitivity, required the sensitized cell to initiate the skin reaction and that the majority of the cellular infiltrate was the result of non-specific host response to injury.

Animals↗

Passive transfer of transplantation immunity. III. Inbred guinea pigs.

Passive transfer of transplantation immunity was accomplished in inbred guinea pigs with tritiated thymidine-labeled lymphoid cells sensitized to homologous tissues. Autoradiographs of the homologous skin graft sites disclosed the presence of relatively few or no labeled cells at the site of rejection. Passive transfer of transplantation immunity was also accomplished with sensitized lymphoid cells enclosed in cell-impenetrable Millipore chambers. Previous studies with passive transfer of tuberculin sensitivity in guinea pigs revealed that the specifically sensitized cells could be easily found at the site of challenge in the presence of specific antigen and were ineffective when enclosed in Millipore chambers. It appeared, then, that the homograft reaction and delayed sensitivity of tuberculin type were achieved by different immunologic mechanisms within the same species.

Animals↗

Passive transfer of transplantation immunity. I. Tritiated lymphoid cells. II. Lymphoid cells in millipore chambers.

Passive transfer of tritiated thymidine labeled lymphoid cells sensitized to homologous tissues into non-sensitized isologous hosts resulted in accelerated rejection of homologous skin grafts in the recipients. Despite 33 per cent label of the suspension, only rare labeled sensitized lymphoid cells could be found at the site of rejection. Passive transfer of sensitized lymphoid cells in millipore chambers implanted subcutaneously or intraperitoneally in non-sensitized isologous hosts resulted in accelerated homograft rejection in the recipients. Transfer of transplantation immunity could not be accomplished with serum from sensitized hosts. The rejection of homologous tissues without the physical presence of the sensitized cell at the graft site suggested that a humoral agent produced by the cell was capable of rejecting the homograft.

Immunity↗