Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection.

Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection. Abstract Text:

Malcolm S Duthie,Maria Kahn,Arsen Zakayan,Maria White,Stuart J Kahn,

Trypanosoma cruzi infection causes Chagas' disease, a chronic inflammatory disease. The specific inflammatory responses that cause Chagas' disease remain unclear, but data argue that parasites that persist in the host stimulate chronic self-damaging immune responses. Because T. cruzi appears to stimulate self-damaging responses, the enthusiasm to develop vaccines that boost antiparasite responses that might increase self-damaging responses has been limited. We previously demonstrated that immunization with a T. cruzi trans-sialidase protein or adoptive transfer of trans-sialidase-specific T-cell clones decreased parasitemia, morbidity, and mortality. Here we report that immunization or adoptive transfer with the protein or clones, before or during T. cruzi infection, boosts the anti-T. cruzi immune response without exacerbating acute or chronic tissue inflammation. These results argue that prophylactic and therapeutic immunotherapy for Chagas' disease can be developed safely.

Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection. Publishing Authors By Initials

MS Duthie,M Kahn,A Zakayan,M White,SJ Kahn,

For similar animals: invertebrates: protozoa: sarcomastigophora: mastigophora: zoomastigophora: kinetoplastida: trypanosomatina: trypanosoma: trypanosoma cruzi research abstracts see: animals: invertebrates: protozoa: sarcomastigophora: mastigophora: zoomastigophora: kinetoplastida: trypanosomatina: trypanosoma: trypanosoma cruzi research

PUBMED ID PMID:

MEDLINE DATE:

Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Clinical and vaccine immunology : CVI

VOLUME: 14

Page Numbers: 1005-12

Journal Abbreviation: Clin. Vaccine Immunol.

ISSN: 1556-6811

DAY: 30

MONTH: 05

YEAR: 2007

Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101252125

Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection. Keywords Mesh Terms:

KEYWORDS: Trypanosoma cruzi

MESH TERMS: pathogenicity

Chemical & Substance for Abstract: Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection. Information

Substance Name: SA85 1.1 antigen, Trypanosoma cruzi

Registry Number: 0

Grant and Affiliation Information for Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection.

AFFILIATION: Infectious Disease Research Institute, 1124 Columbia St., Suite 400, Seattle, WA 98104, USA.

Country: United States

AGENCY: United States NIAID

GRANT: AI48777

ACRONYM: AI

MEDLINETA: Clin Vaccine Immunol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection Related Publications

• BiDil: race medicine or race marketing?
• Does concordance between data sources vary by medical organization type?
• During acute Trypanosoma cruzi infection highly susceptible mice deficient in natural killer cells are protected by a single alpha-galactosylceramide treatment.
• ELMOD2 is an Arl2 GTPase-activating protein that also acts on Arfs.
• Ectopic brown adipose tissue in muscle provides a mechanism for differences in risk of metabolic syndrome in mice.
• Efficacy of slow repetitive transcranial magnetic stimulation in the treatment of resistant auditory hallucinations in schizophrenia: a meta-analysis.
• Entry of US medical school graduates into family medicine residencies: 2006-2007 and 3-year summary.
• Epigenetic and mitochondrial mechanisms in aging and longevity: a report of a meeting of the Longevity Consortium, Napa, California, October 25-27, 2006.
• Essential role of insulin and insulin-like growth factor 1 receptor signaling in cardiac development and function.
• Genetic testing and the future of disability insurance: ethics, law & policy.
• Gestational diabetes mellitus increases the risk of cardiovascular disease in women with a family history of type 2 diabetes.
• Glucose- and time-dependence of islet amyloid formation in vitro.
• HIV prevention costs and program scale: data from the PANCEA project in five low and middle-income countries.
• Human bocavirus infection in young children in the United States: molecular epidemiological profile and clinical characteristics of a newly emerging respiratory virus.
• Interactive effects of a DRD4 polymorphism, lead, and sex on executive functions in children.
• Intra-abdominal fat accumulation predicts the development of the metabolic syndrome in non-diabetic Japanese-Americans.
• Molecular mobility of confined phases in model mesoporous (MCM-41) and microporous (AlPO(4)-5 zeolite) host materials.
• Nautiloid growth rhythms and lunar dynamics (reply).
• Nautiloid growth rhythms and lunar dynamics (reply).
• Nautiloid growth rhythms and lunar dynamics (reply).
• Novel mutations in the respiratory syncytial virus G gene identified in viral isolates from a girl with severe combined immune deficiency treated with intravenous immune globulin.
• On referral patterns for patients with breast cancer.
• Parasite-induced chronic inflammation is not exacerbated by immunotherapy before or during Trypanosoma cruzi Infection.
• Plasma pancreatic polypeptide levels are associated with differences in body fat distribution in human subjects.
• Progressive loss of beta-cell function leads to worsening glucose tolerance in first-degree relatives of subjects with type 2 diabetes.
• Role of suppressors of cytokine signaling SOCS-1 and SOCS-3 in hepatic steatosis and the metabolic syndrome.
• SIRT2 regulates adipocyte differentiation through FoxO1 acetylation/deacetylation.
• Superiority of the Modification of Diet in Renal Disease equation over the Cockcroft-Gault equation in screening for impaired kidney function in Japanese Americans.
• The p85alpha regulatory subunit of phosphoinositide 3-kinase potentiates c-Jun N-terminal kinase-mediated insulin resistance.
• The role of crude human saliva and purified salivary MUC5B and MUC7 mucins in the inhibition of Human Immunodeficiency Virus type 1 in an inhibition assay.