Alteration of immune responses by N-acetylglucosaminyltransferase V during allergic airway inflammation.
Allergol Int
; 60(3): 345-54, 2011 Sep.
Article
in En
| MEDLINE
| ID: mdl-21502802
ABSTRACT
BACKGROUND:
ß-1,6-N-acetylglucosaminyltransferase V (Mgat5 or GlcNac-TV), which is involved in the glycosylation of proteins, is known to be important for down-regulation of TCR-mediated T-cell activation and negatively regulates induction of contact dermatitis and experimental autoimmune encephalomyelitis. However, the role of Mgat5 in the induction of allergic airway inflammation remains unclear.METHODS:
To elucidate the role of Mgat5 in the pathogenesis of allergic airway inflammation, ovalbumin (OVA)-induced airway inflammation was induced in Mgat5-deficient mice. The OVA-specific lymphocyte proliferation and cytokine production levels, OVA-specific IgG1, IgG2a and IgE levels in the serum, and the number of leukocytes and cytokine levels in the bronchoalveolar lavage (BAL) fluid were compared between wild-type and Mgat5-deficient mice.RESULTS:
OVA-specific lymphocyte proliferation and production of IFN-γ and IL-10, but not IL-4, were increased in Mgat5-deficient mice, suggesting that Th2-type immune responses are seemed to be suppressed by increased IFN-γ and IL-10 production in these mice. However, Th2-type responses such as OVA-specific IgG1, but not IgE, and IL-5 levels in BAL fluids were increased in Mgat5-deficient mice. Meanwhile, the number of eosinophils was normal, but the numbers of neutrophils, macrophages and lymphocytes were reduced, in these mutant mice during OVA-induced airway inflammation.CONCLUSIONS:
Mgat5-dependent glycosylation of proteins can modulate acquired immune responses, but it is not essential for the development of OVA-induced eosinophilic airway inflammation.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Respiratory Tract Diseases
/
N-Acetylglucosaminyltransferases
/
Hypersensitivity
Limits:
Animals
Language:
En
Journal:
Allergol Int
Journal subject:
ALERGIA E IMUNOLOGIA
Year:
2011
Document type:
Article
Affiliation country:
Japan