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Erratum |
*
Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh, U.K.;
Department of Biology, Imperial College of Science, Technology and Medicine, London; and
The Rayne Laboratory, Medical School, University of Edinburgh, Edinburgh, United Kingdom.
Abstract
Loss of T lymphocyte proliferation and the emergence of a host
response that is dominated by a Th2-type profile are well-established
features of human filariasis. We have previously reported that adherent
peritoneal exudate cells (PEC) from mice transplanted with adult
Brugia malayi parasites suppress the proliferation of
lymphocytes without blocking Ag-cytokine production in vitro. We now
show that infection of mice with the infective larval (L3) stage of
B. malayi generates a similar population of PEC.
Suppressive cells are generated within 7 days of infection and mediate
their effects through a nitric oxide-independent pathway. Both L3 and
adult infection elicit high levels of host IL-4 whereas the
microfilarial stage of the parasite induces IFN-
production and does
not generate a similar form of suppression. Production of host IL-4 was
necessary to allow the generation of suppressive PEC, given that
IL-4-deficient mice implanted with adult parasites failed to induce
proliferative block. However, IL-10-deficient mice implanted with adult
parasites resulted in T cell suppression, indicating that IL-10 is not
essential for the induction of hyporesponsiveness. Neither IL-4 nor
IL-10 were directly responsible for ablating cellular proliferation in
vitro, as the addition of neutralizing Ab to either cytokine did not
reverse the proliferative block. Thus, IL-4 produced in vivo in
response to filarial L3 and adult parasites is essential for the
induction of proliferative suppression but is not itself the
suppressive factor.
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