Effects of dexamethasone on CTLA-4 expression and apoptosis in lymphocytes obtained from children with mesangial proliferative nephritis.
- Author:
Feng-Ying WANG
1
;
Si-Guang LU
;
Rong-Hua LUO
Author Information
- Publication Type:Journal Article
- MeSH: Antigens, CD; blood; Apoptosis; drug effects; CTLA-4 Antigen; Child; Dexamethasone; pharmacology; Female; Glomerulonephritis, Membranoproliferative; drug therapy; etiology; Humans; Lymphocytes; drug effects; immunology; Male
- From: Chinese Journal of Contemporary Pediatrics 2009;11(12):957-960
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEThe pathogenesis of mesangial proliferative glomerulonephritis (MsPGN) and mechanisms of glucocorticoid (GC) resistance have not been fully identified. Cytotoxic T-lymphocyte antigen-4 (CTLA-4) is an important inhibitor of T-lymphocyte activation. The objective of the study is to investigate the CTLA-4 expression and apoptosis in lymphocytes of children with MsPGN and the effects of dexamethasone (Dex) on the CTLA-4 expression and apoptosis.
METHODSBlood samples were collected from 36 children with MsPGN and 30 healthy children. CTLA-4 expression in in vitro cultured lymphocytes with or without Dex treatment was measured by flow cytometry following direct immune fluorescene. The rate of apoptosis in the lymphocytes was evaluated by annexin V-FITC and propidium iodide staining.
RESULTSThe CTLA-4 expression and apoptosis in lymphocytes from children with MsPGN were significantly lower than those in the healthy control children in the absence or presence of Dex treatment (p<0.05). There was a positive correlation between CTLA-4 expression and apoptosis in lymphocytes (p<0.05).
CONCLUSIONSAbnormal CTLA-4 expression may participate in the pathogenesis of MsPGN and be one of mechanisms of GC resistance.
