On the mechanism of urethan leukemogenesis in newborn C57BL mice. I. Influence of injections of syngeneic bone marrow cell suspensions.
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Biomedical subjects
Publications and source records attributed to N Trainin.
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The effect of thymus humoral factor (THF) on T cell growth factor (TCGF) production by T cells and the association between splenic macrophages and T cells from young (2-3 months) and old (20-24 months) mice in this respect were studied. Splenocytes were divided into three groups: stimulated with concanavalin A (Con A); preincubated with THF and then stimulated with Con A; or stimulated with Con A and thereafter incubated with THF. These cells were then examined for production of TCGF. Cells treated with Con A and THF as described above were passed on nylon wool to enrich T cell populations and added to mitogen-sensitized (Con A or lipopolysaccharide) adherent splenocytes of old and young mice in the following combinations: young adherent and young T cells; young adherent and old T cells; old adherent and young T cells; and old adherent and old T cells. The results demonstrated that: (A) cells of old mice produced less TCGF than the young; (B) preincubation of splenocytes or nylon-wool enriched T cells with THF increased the production of TCGF consistently in young mice, whereas in the old a significant increase was observed only in some cases; (C) depressed TCGF activity was observed when treatment with THF to splenocytes or nylon-wool enriched T cells from young and old mice was performed after Con A stimulation, and this was also more pronounced in the young; (D) the reduced level of TCGF in the old seemed to be related to a lesion in the T cell compartment, since adherent cells from old and young mouse spleens could support TCGF production by T cells from young mice and not from old.
Immunostimulation with complete Freund adjuvant (CFA) reverses the tendency to fetal loss in the CBA/J x DBA/2J mouse. First attempts to understand the mechanisms underlying this effect were to evaluate phenotypic and functional changes in the lymphocytic cell population after immunopotentiation. We demonstrated that treatment with CFA leads to diminished responses of maternal splenocytes towards paternal alloantigens and this low response cannot be improved with exogenous interleukin-2. Lymphocytes derived from spleen, para-aortic draining lymph nodes and placenta significantly suppress maternal response to paternal antigens. The effect of low fetal resorption rate is followed by marked elevation of asialo GM-1 and HNK-1-positive cells but not followed by any change of the L3T4 or Lyt-2-positive lymphocyte population in either the spleen or in draining lymph nodes. L3T4 and Lyt-2-positive cells have not been found in the placenta. An important feature was marked elevation of Mac-1-positive cells in the placentas of CFA-treated animals. The relevance of these findings to CFA-induced fetal protection is still under investigation.
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Intracellular cAMP was measured in peripheral blood mononuclear cells from patients with ankylosing spondylitis and from controls. The effect of thymic humoral factor (THF) on T lymphocyte cAMP content was monitored in both groups to determine if there were any differences in immature T cell proportions. Equivalent cAMP levels were found in patients and controls in the absence of THF and again after stimulation with this immune modulator.