The systemic immune response of BALB/c mice infected with larval Taenia crassiceps is a mixed Th1/Th2-type response

Abstract

The subsets of lymphocytes and cytokines regulating the site-specific immune response in experimental cysticercosis (Taenia crassiceps) are not known. This study investigated the cells present at the site of infection (PECs) using flow cytometry and measured the cytokines produced by these cells through 50 days of infection. The results showed an expansion of B220+CD5+, B220+CD5-, alpha beta TCR+CD4+ and CD8+ cells coincident with a transient increase in IL-10 production. After the initial increase, the percentage of B220+CD5- and helper T cells decreased with a concomitant decrease in IL-10 production. CD8+ T cells continued to increase throughout infection and gamma delta TCR+ cells increased after 10 days of infection. PECs demonstrated an increased IFN-gamma and IL-4 production throughout infection when stimulated with larval antigens. Because a Th2-type polarization has been shown for spleen cells from infected BALB/c mice, cytokine profiles of spleen cells and PECs in response to ConA and larval antigens were compared. ConA and antigen-specific stimulation of spleen cells from 50-day-infected mice produced increased amounts of IL-10 while PECs showed a decreased IL-10 production suggesting that anatomically distinct lymphoid populations produce different cytokines and promote different types of responses. Surprisingly, late in infection the levels of IL-4 and IFN-gamma in serum increased substantially (460-fold and 100-fold, respectively). The systemic immune response of BALB/c mice during experimental cysticercosis, therefore, is a mixed Th1/Th2-type response.

Cutting Edge: Susceptibility to the Larval Stage of the Helminth ParasiteTaenia crassicepsIs Mediated by Th2 Response Induced Via STAT6 Signaling

“…Although it is widely accepted that Th2-like response mediates protective immunity against most helminths (5), its role in mediating protection against murine cysticercosis is not clear (6).…”

Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis

“…Soon afterwards there is a strong Th2 polarization due to the immunoregulatory capacity of the parasite increasing serum levels of IgG and IgE as well as IL-4, IL-13 and IL-5, which inhibits the initial Th1 response and favors the growth of parasitic burden 7,8,10,11 . The experimental models exploring the neurological location of cysticerci are described using Mesocestoides corti 5,12,13 and T. crassiceps 6 . The model carried out with M. corti was used to describe the role of defense cells and cytokines in the host-parasite relationship 13 , the expression of Toll-like receptors 5 , the migration of leucocytes to the central nervous system, the junction complex proteins and the immune system evasion strategies 14 .…”

Cysticercosis and the immunossupression: what are the mechanisms involved?

“…There are only few studies available regarding aspects of the cellular immune response, most of them showing immunosuppression in humans 4 , pigs 5 , and in experimental mouse models [6][7][8][9] . A study from our group using a lymphoproliferation assay with T. solium and T. crassiceps antigens as stimuli showed an antigen-specific suppression in NC-patients, suggesting that the antigenic components play a suppressor role in the host immune response 10 .…”

“…The immunosuppression observed in experimental cysticercosis seems to be related to the cytokine profile 8,[13][14][15] . Our contribution in this field showed that by using T. solium antigen as stimuli, there is a predominance of Th1 response in inflammatory NC-patients and a mixed Th1/Th2 pattern in noninflammatory NC-patients 12 .…”

“…Some experimental cysticercosis studies have attempted to determine the causes of immunosuppression: release of antigenic products 16 that form circulating immunocomplexes 17 , suppressing lymphocyte cytokine production or inducing chromosome instability 18 ; increase and/or decrease in CD8 cells depending on the evolution phase of the disease 19 ; genetic instability and chromosome alterations in circulating lymphocytes induced by infection 20,21 ; macrophages with activity involving the programmed death ligand 1 pathway 7 ; and Th1 and/or Th2 cytokines 6,8,9,[13][14][15]22,23 . Recently, it was reported the Toll-like receptor 2-dependent pathways as involved in the recognition of T. crassiceps, with subsequent activation of the innate response and production of the inflammatory cytokines 24 .…”