The infection developed by Wistar Furth rats inoculated with the Y strain of Trypanosoma cruzi was the experimental model used in our study. The results showed that this infection altered considerably the CD4/CD8 lymphocyte subset ratio and the natural cytotoxic activity of mononuclear cells in the spleen, blood, and myocardial tissue. Concomitantly, an expansion of the number of cells expressing major histocompatibility complex (MHC) class II antigens was observed, as well as spontaneous development of high levels of blast cells, mainly in the spleen. The inflammatory infiltration of the myocardium, made up essentially of CD8+ cells (cytotoxic/suppressor T cells, natural killer cells), was initially found at 9 days postinfection, spread continuously, and was observed until the death of the animals at about 18 days postinfection. T. cruzi infection also enhanced the natural killer activity of mononuclear cells in the blood, spleen, and myocardium. Sorting these cells by affinity columns showed that the natural killer function was performed exclusively by the CD8+ population, which did not express MHC class II antigens. It was shown that the polyclonal T-lymphocyte activation induced by T. cruzi infection results in a wide distribution of CD8+ cells with enhanced natural cytotoxic activity in the spleen, blood, and cardiac tissue.
The immunomodulatory effect of cimetidine (CIM), a histamine type-2 receptor antagonist, was evaluated in respect to the blastogenic response to Con A of Wistar Furth (WF) rats infected by the Y strain of Trypanosoma cruzi (T. cruzi). Enhancement of blastogenesis of normal splenocytes was observed at a concentration of 10-3M. However, the splenocytes from infected animals responded to concentrations of CIM ranging from 10-8 to 10-3M. The mitogenic response to Con A of cells from infected animals was restored in the presence of CIM. The results show that CIM modulates the "in vitro" proliferative response of cells from T. cruzi-infected rats and suggest an immunoregulatory role of histamine and/or of cells that express H2 receptors in this infection.
To evaluate the immunological properties of aluminum (Al) in experimental Al intoxication in rats, we performed heart transplantation and in vitro experiments. Lewis (Lew) rats were intoxicated with intraperitoneal injections of AlCl3. heart transplants were performed using Brown-Norway (BN) rats as donors. Isotransplants and normal Lew were used as controls. No differences in survival were observed. Unidirectional mixed lymphocyte cultures (MLC) and Concanavalin A (Con A)-stimulated cultures were prepared using spleen cells from normal and Al-intoxicated Lew rats. No differences were found in unidirectional MLC. Intoxicated cells showed a less intense response to con A than did normal cells. In conclusion, we could not detect an immunosuppressive role of Al intoxication in experimental cardiac transplantation or in MLC. However, the depressed Con A blastogenic response of Al-intoxicated cells may reflect an immunological role yet to be defined.
In the present work the kinetics of class II MHC expression on OX8+ lymphocytes generated by skin allograft and its relationship to the lytic activity were studied. Mononuclear cells from the spleen of LEW (RT1(1) rats bearing BN (RT1n) skin graft for 3, 5 or 7 days were sorted out by sequential immune affinity using columns of Degalan-V26 beads treated with anti-rat or anti-mouse Ig. After depletion of B cells, T cells were precoated with W3/25 MoAb (anti-CD4 equivalent) and sorted out using an anti-mouse Ig column. The W3/25-/OX8+ cells (CD8 equivalent) were then coated with OX4 MoAb (anti-RT1.B) or murine A.TH anti-A.TL alloantiserum (anti I-E, cross-reacts with RT1.D) and were passed through a new anti-mouse Ig column in order to obtain the four subpopulations, RT1.B+, .B-, .D+ and .D-. Their specific lytic activity against BN Con A-stimulated cells increased from the 3rd to the 7th d after the skin graft. The lytic activity observed on the 3rd and 5th d was associated with all four subpopulations analyzed. In contrast, on the 7th d, the lytic activity was concentrated in the RT1.B+ subpopulation. These results, associated with the increase in the number of OX8+/RT1.B+ cells along with days after graft, suggest that RT1.B expression is not essential but is associated with the effectiveness of the cytotoxic activity. It is also possible that RT1.B expression is a marker of cytotoxic T-cell differentiation.
To evaluate the immunological properties of aluminum (Al) in experimental Al intoxication in rats, we performed heart transplantation and in vitro experiments. Lewis (Lew) rats were intoxicated with intraperitoneal injections of AlCl3. heart transplants were performed using Brown-Norway (BN) rats as donors. Isotransplants and normal Lew were used as controls. No differences in survival were observed. Unidirectional mixed lymphocyte cultures (MLC) and Concanavalin A (Con A)-stimulated cultures were prepared using spleen cells from normal and Al-intoxicated Lew rats. No differences were found in unidirectional MLC. Intoxicated cells showed a less intense response to con A than did normal cells. In conclusion, we could not detect an immunosuppressive role of Al intoxication in experimental cardiac transplantation or in MLC. However, the depressed Con A blastogenic response of Al-intoxicated cells may reflect an immunological role yet to be defined.
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