transforming-growth-factor-beta and Helminthiasis--Animal

transforming-growth-factor-beta has been researched along with Helminthiasis--Animal* in 2 studies

Reviews

1 review(s) available for transforming-growth-factor-beta and Helminthiasis--Animal

ArticleYear
Immune modulation by helminth parasites of ruminants: implications for vaccine development and host immune competence.
    Parasite (Paris, France), 2014, Volume: 21

    Parasitic helminths reside in immunologically-exposed extracellular locations within their hosts, yet they are capable of surviving for extended periods. To enable this survival, these parasites have developed complex and multifaceted mechanisms to subvert or suppress host immunity. This review summarises current knowledge of immune modulation by helminth parasites of ruminants and the parasite-derived molecules involved in driving this modulation. Such immunomodulatory molecules have considerable promise as vaccine targets, as neutralisation of their function is predicted to enhance anti-parasite immunity and, as such, current knowledge in this area is presented herein. Furthermore, we summarise current evidence that, as well as affecting parasite-specific immunity, immune modulation by these parasites may also affect the ability of ruminant hosts to control concurrent diseases or mount effective responses to vaccination.

    Topics: Animals; Apyrase; Cathepsin L; Fasciola hepatica; Fascioliasis; Galectins; Helminth Proteins; Helminthiasis, Animal; Host-Parasite Interactions; Immunocompetence; Intestinal Diseases, Parasitic; Macrophage Migration-Inhibitory Factors; Peroxiredoxins; Rumen; Ruminants; Stomach Diseases; Transforming Growth Factor beta; Vaccination; Vaccines

2014

Other Studies

1 other study(ies) available for transforming-growth-factor-beta and Helminthiasis--Animal

ArticleYear
Intestinal helminths regulate lethal acute graft-versus-host disease and preserve the graft-versus-tumor effect in mice.
    Journal of immunology (Baltimore, Md. : 1950), 2015, Feb-01, Volume: 194, Issue:3

    Donor T lymphocyte transfer with hematopoietic stem cells suppresses residual tumor growth (graft-versus-tumor [GVT]) in cancer patients undergoing bone marrow transplantation (BMT). However, donor T cell reactivity to host organs causes severe and potentially lethal inflammation called graft-versus-host disease (GVHD). High-dose steroids or other immunosuppressive drugs are used to treat GVHD that have limited ability to control the inflammation while incurring long-term toxicity. Novel strategies are needed to modulate GVHD, preserve GVT, and improve the outcome of BMT. Regulatory T cells (Tregs) control alloantigen-sensitized inflammation of GVHD, sustain GVT, and prevent mortality in BMT. Helminths colonizing the alimentary tract dramatically increase the Treg activity, thereby modulating intestinal or systemic inflammatory responses. These observations led us to hypothesize that helminths can regulate GVHD and maintain GVT in mice. Acute GVHD was induced in helminth (Heligmosomoides polygyrus)-infected or uninfected BALB/c recipients of C57BL/6 donor grafts. Helminth infection suppressed donor T cell inflammatory cytokine generation and reduced GVHD-related mortality, but maintained GVT. H. polygyrus colonization promoted the survival of TGF-β-generating recipient Tregs after a conditioning regimen with total body irradiation and led to a TGF-β-dependent in vivo expansion/maturation of donor Tregs after BMT. Helminths did not control GVHD when T cells unresponsive to TGF-β-mediated immune regulation were used as donor T lymphocytes. These results suggest that helminths suppress acute GVHD using Tregs and TGF-β-dependent pathways in mice. Helminthic regulation of GVHD and GVT through intestinal immune conditioning may improve the outcome of BMT.

    Topics: Acute Disease; Adoptive Transfer; Animals; Bone Marrow Transplantation; Cytokines; Disease Models, Animal; Graft vs Host Disease; Helminthiasis, Animal; Helminths; Immunomodulation; Immunophenotyping; Intestines; Male; Mice; Neoplasms; T-Lymphocyte Subsets; T-Lymphocytes, Regulatory; Transforming Growth Factor beta; Transplantation Conditioning; Transplantation, Homologous

2015
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