Human Leucocyte Antigen-G (HLA-G) and Its Murine Functional Homolog Qa2 in the Trypanosoma cruzi Infection. (20th January 2015)
- Record Type:
- Journal Article
- Title:
- Human Leucocyte Antigen-G (HLA-G) and Its Murine Functional Homolog Qa2 in the Trypanosoma cruzi Infection. (20th January 2015)
- Main Title:
- Human Leucocyte Antigen-G (HLA-G) and Its Murine Functional Homolog Qa2 in the Trypanosoma cruzi Infection
- Authors:
- Dias, Fabrício C.
Mendes-Junior, Celso T.
Silva, Maria C.
Tristão, Fabrine S. M.
Dellalibera-Joviliano, Renata
Moreau, Philippe
Soares, Edson G.
Menezes, Jean G.
Schmidt, André
Dantas, Roberto O.
Marin-Neto, José A.
Silva, João S.
Donadi, Eduardo A. - Other Names:
- Bozza Marcelo T. Academic Editor.
- Abstract:
- Abstract : Genetic susceptibility factors, parasite strain, and an adequate modulation of the immune system seem to be crucial for disease progression after Trypanosoma cruzi infection. HLA-G and its murine functional homolog Qa2 have well-recognized immunomodulatory properties. We evaluated the HLA-G 3′ untranslated region (3′UTR) polymorphic sites (associated with mRNA stability and target for microRNA binding) and HLA-G tissue expression (heart, colon, and esophagus) in patients presenting Chagas disease, stratified according to the major clinical variants. Further, we investigated the transcriptional levels of Qa2 and other pro- and anti-inflammatory genes in affected mouse tissues during T. cruzi experimental acute and early chronic infection induced by the CL strain. Chagas disease patients exhibited differential HLA-G 3′UTR susceptibility allele/genotype/haplotype patterns, according to the major clinical variant (digestive/cardiac/mixed/indeterminate). HLA-G constitutive expression on cardiac muscle and colonic cells was decreased in Chagasic tissues; however, no difference was observed for Chagasic and non-Chagasic esophagus tissues. The transcriptional levels of Qa2 and other anti and proinflammatory ( CTLA-4, PDCD1, IL-10, INF- γ, and NOS-2 ) genes were induced only during the acute T. cruzi infection in BALB/c and C57BL/6 mice. We present several lines of evidence indicating the role of immunomodulatory genes and molecules in human and experimental T. cruziAbstract : Genetic susceptibility factors, parasite strain, and an adequate modulation of the immune system seem to be crucial for disease progression after Trypanosoma cruzi infection. HLA-G and its murine functional homolog Qa2 have well-recognized immunomodulatory properties. We evaluated the HLA-G 3′ untranslated region (3′UTR) polymorphic sites (associated with mRNA stability and target for microRNA binding) and HLA-G tissue expression (heart, colon, and esophagus) in patients presenting Chagas disease, stratified according to the major clinical variants. Further, we investigated the transcriptional levels of Qa2 and other pro- and anti-inflammatory genes in affected mouse tissues during T. cruzi experimental acute and early chronic infection induced by the CL strain. Chagas disease patients exhibited differential HLA-G 3′UTR susceptibility allele/genotype/haplotype patterns, according to the major clinical variant (digestive/cardiac/mixed/indeterminate). HLA-G constitutive expression on cardiac muscle and colonic cells was decreased in Chagasic tissues; however, no difference was observed for Chagasic and non-Chagasic esophagus tissues. The transcriptional levels of Qa2 and other anti and proinflammatory ( CTLA-4, PDCD1, IL-10, INF- γ, and NOS-2 ) genes were induced only during the acute T. cruzi infection in BALB/c and C57BL/6 mice. We present several lines of evidence indicating the role of immunomodulatory genes and molecules in human and experimental T. cruzi infection. … (more)
- Is Part Of:
- Mediators of inflammation. Volume 2015(2015)
- Journal:
- Mediators of inflammation
- Issue:
- Volume 2015(2015)
- Issue Display:
- Volume 2015, Issue 2015 (2015)
- Year:
- 2015
- Volume:
- 2015
- Issue:
- 2015
- Issue Sort Value:
- 2015-2015-2015-0000
- Page Start:
- Page End:
- Publication Date:
- 2015-01-20
- Subjects:
- Inflammation -- Mediators -- Periodicals
Biological response modifiers -- Periodicals
Inflammation (Pathologie) -- Médiateurs
Immunomodulateurs
Biological response modifiers
Inflammation -- Mediators
Immunology
Autacoids
Immunologic Factors
Cell Adhesion Molecules
Cell Communication
Cytokines
Inflammation
Periodicals
Electronic journals
616.0473 - Journal URLs:
- https://www.hindawi.com/journals/mi/ ↗
- DOI:
- 10.1155/2015/595829 ↗
- Languages:
- English
- ISSNs:
- 0962-9351
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 23514.xml