Influence of intrapulmonary regulatory peptides on the expressions of HLA-DR, CD80 and CD86 in human bronchial epithelial cells..
- Author:
Li-Hua PENG
1
;
Xiao-Qun QIN
;
Yu-Rong TAN
;
Yang XIANG
;
Hui-Jun LIU
Author Information
1. Department of Physiology, Xiangya Medical School, Central South University, Changsha, China.
- Publication Type:Journal Article
- MeSH:
Antigen-Presenting Cells;
metabolism;
B7-1 Antigen;
metabolism;
B7-2 Antigen;
metabolism;
Bronchi;
cytology;
Calcitonin Gene-Related Peptide;
pharmacology;
Epithelial Cells;
metabolism;
HLA-DR Antigens;
metabolism;
Humans;
Ozone;
adverse effects;
Vasoactive Intestinal Peptide;
pharmacology
- From:
Acta Physiologica Sinica
2008;60(6):723-729
- CountryChina
- Language:Chinese
-
Abstract:
Antigen presenting is the initial step of the immune responses. In order to verify that human bronchial epithelial cells (HBECs) can express antigen presentation molecules, which can be modulated by intrapulmonary regulatory peptides, the present study was designed to examine the expressions of human leukocyte antigen DR (HLA-DR), CD80 and CD86 in resting or ozone-stressed HBECs by using immunocytochemistry and flow cytometry analysis. The results showed that HBECs expressed HLA-DR, CD80 and the expressions of HLA-DR and CD80 molecules were down-regulated under ozone stress. While VIP, P3513 and CGRP upregulated the expression of HLA-DR in resting or ozone-stressed HBECs, they had different effects on CD80 expression. VIP did not influence the expression of CD80 under resting state, but increased the expression of CD80 under ozone stress. CGRP decreased CD80 expression in resting HBECs, but increased CD80 expression in ozone-stressed HBECs. P3513 increased CD80 expression in resting HBECs, but decreased CD80 expression in ozone-stressed HBECs. The expression of CD86 was absent in resting or ozone-stressed HBECs. The results obtained demonstrate that HBECs have the capability to act as antigen presenting cells and the expression of HLA-DR and costimulatory molecules can be modulated by intrapulmonary regulatory peptides.
