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D Ilfeld

Publications and source records attributed to D Ilfeld.

30 records · Page 2Linked to original sources

Correction of a suppressor cell deficiency in familial Mediterranean fever by colchicine.

We have previously reported a suppressor cell deficiency in four patients with familial Mediterranean fever (FMF). Since colchicine prevents FMF attacks, we tested the effect of colchicine (1 mg twice daily) on the suppressor cell function in three of these FMF patients. Proliferation of phytohaemagglutinin-stimulated responder cells co-cultured with concanavalin A-induced suppressor cells was measured. The three FMF patients' means (+/- s.e.m.) percentage suppression of normal responder cells was markedly low before treatment (6 +/- 2) but significantly (P less than 0.001) increased during colchicine treatment (41 +/- 5) to levels similar to normal volunteers' mean percentage suppression (44 +/- 3). Colchicine corrected their suppressor cell deficiency and prevented FMF attacks during the 15 months of treatment. These findings support the hypothesis that there may be an association between these three patients' suppressor cell deficiency and the pathogenesis of their disease. Furthermore, colchicine may be potentially useful in treating patients with other diseases associated with a suppressor cell deficiency.

Adult↗

Effects of concanavalin A-stimulated spleen cell supernate on the redevelopment of autoimmunity in NZB/NZW mice in induced remission.

Because female NZB/NZW mice develop autoimmune abnormalities similar to those encountered in human systemic lupus erythematosus (SLE), a group of female NZB/NZW mice were used to study mechanisms of autoimmunity. These mice were treated daily with an immune suppressive material, 0.5 ml of a concanavalin A-stimulated spleen cell supernate (CONS), starting at 30 weeks of age after induced remission with prednisolone. This CONS treatment effectively reduced the proteinuria and the severity of the renal lesions, but failed to reduce the serum anti-DNA antibody level. Thus, the CONS effect on the autoimmunity in the NZB/NZW mice in induced remission appears to result from a more complicated mechanism than reduction in serum anti-DNA antibody level.

Animals↗

The role of thymus on autosensitization against syngeneic normal and malignant cells.

Mouse lymphocytes were exposed to syngeneic fibroblasts and tumor cells in Millipore chambers inserted into the peritoneal cavity of intact and thymectomized mice. Autosensitization to fibroblasts occurred only if the chambers were carried by thymectomized mice. Sensitization to tumor-specific antigens also took place in intact mice. If thymic extract was administered to thymectomized mice autosensitization in the chambers was inhibited.

Animals↗

Increased reactivity of mouse spleen cells sensitized in vitro against syngeneic tumor cells in the presence of a thymic humoral factor.

Unprimed mouse spleen cells cultured in vitro on syngeneic tumor cell monolayers have been previously shown to become specifically sensitized and to mediate cytotoxicity against the same type of tumor cells. This complete in vitro system of cell-mediated response has been presently used to test the effect of a thymic humoral factor (THF) upon the differentiation process leading to the generation of specifically committed lymphocytes. Culture media were supplemented with 2% THF during either the sensitization or effector phase, or both phases of the reaction. Whereas the addition of THF during both phases or during sensitization only resulted in a significant increase in the cytotoxicity index, THF added during the effector phase was ineffective. The behavior of unsensitized spleen cells and of spleen cells sensitized against nonrelated transplantation antigens remained unmodified by THF. After showing that the entire reaction is mediated by lymphocytes of thymic origin, THF was directly tested on T or B spleen cells. It was found that only T cells reacted to THF by an increased cytotoxic capacity, while B cells remained inactive after addition of THF. It was therefore concluded that THF activates a postthymic population of lymphoid cells, transforming them into fully competent lymphocytes.

Animals↗