Experimental Trypanosoma brucei infections selectively suppress both interleukin 2 production and interleukin 2 receptor expression.
Experimental infections with Trypanosoma brucei AnTat 1.1.E not only account for a suppression of interleukin 2 (IL 2) production, but also induce an impairment of IL 2 receptor expression. Indeed, lymph node cells derived from infected mice failed to express IL 2 receptors following mitogenic stimulation as compared to normal controls. This impairment was not attributed to a modulation of the number of T cells and was not caused by the presence of living parasites. Furthermore, the basal level of IL 2 receptor expression could not be re-established through the exogenous supply of recombinant IL 2. This impairment of receptor expression was found to be mediated by suppressive cells that affect the relative number of receptor-positive cells as well as the mean receptor density. On the other hand, the mitogen-induced secretion of other T cell-derived lymphokines was not inhibited during infection, indicating that the severe suppression of IL 2 regulation was not attributed to a total paralysis of the T cell responsiveness.
D000818:Animals; D007376:Interleukin-2 / Q000096:biosynthesis*; D008262:Macrophage Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D011971:Receptors, Immunologic / Q000096:biosynthesis*; D015375:Receptors, Interleukin-2; D014346:Trypanosoma brucei brucei; D014353:Trypanosomiasis, African / Q000276:immunology / Q000378:metabolism*
D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2