Interleukin 10 and dendritic cells are the main suppression mediators of regulatory T cells in human neurocysticercosis

Neurocysticercosis is a clinically and radiologically heterogeneous disease, ranging from asymptomatic infection to a severe, potentially fatal clinical picture. The intensity and extension of the parasite-elicited inflammatory reaction is a key factor for such variability. The main features of the inflammatory process found in the brain and in the peripheral blood of neurocysticercosis patients will be discussed in this review, and the factors involved in its modulation will be herein presented.

Section: Inflammation and Host Factorsmentioning

confidence: 87%

Immunopathology in Taenia solium neurocysticercosis

Fleury

Cárdenas

Adalid‐Peralta

et al. 2016

“…Th1 and Th17 populations are usually associated with host pathology, contrary to Th2 response and expansion of regulatory T cells (Treg) which suggest asymptomatic or mild infection 5 . For example, symptomatic NCC is linked to increased serum levels of proinflammatory cytokines 6 while Th2/Treg milieu is related to asymptomatic NCC 6‐9 . However, it is not very clear how the host immune response is influenced by the cysts present directly in the CNS and those disseminated in other body parts.…”

Section: Introductionmentioning

confidence: 99%

The peripheral immune response of mice infected with a neuropathogenic schistosome

Majer

Macháček

Súkeníková

et al. 2020

Helminths do often invade the central nervous system (CNS) of vertebrates, including humans, causing severe pathologies, such as in the case of neurocysticercosis (NCC) or neurotoxocarosis. 1 Although the CNS was formerly considered an immune-privileged site with a limited capacity to develop an adaptive immune response, this view has recently been revisited. 2,3 Inflammatory cells are recruited into the infected CNS as well as pathogen-specific T cells, which were primed in the periphery. 4 The polarization of helminth-specific T helper (Th) cells largely orchestrates the host immune response. Th1 and Th17 populations are usually associated with host pathology, contrary to Th2 response and expansion of regulatory T cells (Treg) which suggest asymptomatic or mild infection. 5 For example, symptomatic NCC is linked to increased serum levels of proinflammatory cytokines 6 while Th2/ Treg milieu is related to asymptomatic NCC. 6-9 However, it is not very clear how the host immune response is influenced by the cysts present directly in the CNS and those disseminated in other body parts. The same applies to Toxocara spp. which exhibits a marked Abstract Trichobilharzia regenti (Schistosomatidae) percutaneously infects birds and mammals and invades their central nervous system (CNS). Here, we characterized the peripheral immune response of infected mice and showed how it was influenced by the parasite-induced inflammation in the skin and the CNS. As revealed by flow cytometry, T cells expanded in the spleen and the CNS-draining lymph nodes 7-14 days post-infection. Both T-bet+ and GATA-3+ T cells were markedly elevated suggesting a mixed type 1/2 immune response. However, it dropped after 7 dpi most likely being unaffected by the neuroinflammation. Splenocytes from infected mice produced a high amount of IFN-γ and, to a lesser extent, IL-10, IL-4 and IL-17 after in vitro stimulation by cercarial homogenate. Nevertheless, it had only a limited capacity to alter the maturation status of bone marrow-derived dendritic cells (BMDCs), contrary to the recombinant T. regenti cathepsin B2, which also strongly augmented expression of Ccl5, Cxcl10, Il12a, Il33 and Il10 by BMDCs. Taken together, mice infected with T. regenti developed the mixed type 1/2 immune response, which was driven by the early skin inflammation rather than the late neuroinflammation. Parasite peptidases might play an active role in triggering the host immune response. K E Y W O R D S cathepsin B, central nervous system, dendritic cells, lymph nodes, skin, spleen, T lymphocytes

“…79 In human NCC, Foxp3 + regulatory T cells are also important. 150,151 These cells express enhanced levels of PD-1, the negative costimulation receptor CTLA-4 and further suppressive receptors.…”

Section: How Do L Arval Taeniids E Vade G R Anulomatous Re S P Ons mentioning

confidence: 99%

Granulomatous responses in larval taeniid infections

Díaz

Sagasti

Casaravilla

2018

Granulomas are responses to persistent nonliving bodies or pathogens, centrally featuring specialized macrophage forms called epithelioid and multinucleated giant cells. The larval stages of the cestode parasites of the Taeniidae family (Taenia, Echinococcus) develop for years in fixed tissue sites in mammals. In consequence, they are targets of granulomatous responses. The information on tissue responses to larval taeniids is fragmented among host and parasite species and scattered over many decades. We attempt to draw an integrated picture of these responses in solid tissues. The intensity of inflammation around live parasites spans a spectrum from minimal to high, parasite vitality correlating with low inflammation. The low end of the inflammatory spectrum features collagen capsules proximal to the parasites and moderate distal infiltration. The middle of the spectrum is dominated by classical granulomatous responses, whereas the high end features massive eosinophil invasions. Across the range of parasite species, much observational evidence suggests that eosinophils are highly effective at killing larval taeniids in solid tissues, before and during chronic granulomatous responses. The evidence available also suggests that these parasites are adapted to inhibit host granulomatous responses, in part through the exacerbation of host regulatory mechanisms including regulatory T cells and TGF-β.