Immunosuppression by aldicarb of T cell responses to antigen-specific and polyclonal stimuli results from defective IL-1 production by the macrophages

Toxicol Appl Pharmacol. 1990 Dec;106(3):408-17. doi: 10.1016/0041-008x(90)90336-s.


In the present study we investigated the immunomodulatory effects of aldicarb, a carbamate pesticide, on T cells activated by a number of different ways. When C3H mice were injected intraperitoneally with a single dose of Aldicarb, 0.005-50 micrograms/kg body wt, and their spleen cells were stimulated with T cell mitogens such as concanavalin A (ConA)3 or anti-CD3 monoclonal antibodies (mAb), a decreased responsiveness was detected when compared to the control mice. Aldicarb administered at concentrations less than 0.005 microgram/kg body wt failed to cause significant immunosuppression. Interestingly, when purified T cells from immunosuppressive doses of aldicarb-treated mice were stimulated with ConA in the presence of irradiated control macrophages, the defective T cell response was no longer demonstrable. Also, purified control T cells stimulated with ConA in the presence of irradiated macrophages from aldicarb-treated mice showed decreased responsiveness. Similar observations were made using anti-CD3 mAb to activate the T cells, inasmuch as whole spleen cells from aldicarb-treated mice showed decreased responsiveness to anti-CD3 stimulation, whereas purified T cells in the presence of irradiated control macrophages showed normal reactivity. The fact that aldicarb did not directly affect the T cell functions was further confirmed by stimulating purified T cells from aldicarb-treated mice with phorbol myristate acetate and calcium ionophore, a response which is independent of the accessory cells and which was found to be normal in aldicarb-treated mice. It was observed that the macrophages from aldicarb-treated mice demonstrated a decreased capacity to stimulate conalbumin-specific T helper cell clone, D10.G4, and when activated produced decreased amounts of IL-1 when compared to control macrophages. Also, the decreased stimulation of D10.G4 clone by aldicarb-treated macrophages was reconstituted when exogenous recombinant IL-1 was added to the cultures. These data together suggested that aldicarb affects the macrophage functions by interfering with IL-1 production and that it does not affect the T cell functions directly.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aldicarb / toxicity*
  • Animals
  • Antibodies, Monoclonal / immunology
  • Female
  • Immunosuppression Therapy
  • Interleukin-1 / biosynthesis
  • Interleukin-2 / biosynthesis*
  • Lymphocyte Activation
  • Macrophages / metabolism*
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Mitogens / pharmacology
  • Spleen / cytology
  • Spleen / drug effects
  • T-Lymphocytes / drug effects*


  • Antibodies, Monoclonal
  • Interleukin-1
  • Interleukin-2
  • Mitogens
  • Aldicarb