PMID- 23327606 OWN - NLM STAT- MEDLINE DCOM- 20130711 LR - 20211021 IS - 1465-993X (Electronic) IS - 1465-9921 (Print) IS - 1465-9921 (Linking) VI - 14 IP - 1 DP - 2013 Jan 18 TI - Human leukocyte antigen-G expression in differentiated human airway epithelial cells: lack of modulation by Th2-associated cytokines. PG - 4 LID - 10.1186/1465-9921-14-4 [doi] AB - BACKGROUND: Human leukocyte antigen (HLA)-G is a nonclassical class I antigen with immunomodulatory roles including up-regulation of suppressor T regulatory lymphocytes. HLA-G was recently identified as an asthma susceptibility gene, and expression of a soluble isoform, HLA-G5, has been demonstrated in human airway epithelium. Increased presence of HLA-G5 has been demonstrated in bronchoalveolar lavage fluid recovered from patients with mild asthma; this suggests a role for this isoform in modulating airway inflammation though the mechanisms by which this occurs is unclear. Airway inflammation associated with Th2 cytokines such as IL-4 and IL-13 is a principal feature of asthma, but whether these cytokines elicit expression of HLA-G is not known. METHODS: We examined gene and protein expression of both soluble (G5) and membrane-bound (G1) HLA-G isoforms in primary differentiated human airway epithelial cells collected from normal lungs and grown in air-liquid interface culture. Cells were treated with up to 10 ng/ml of either IL-4, IL-5, or IL-13, or 100 ng/ml of the immunomodulatory cytokine IL-10, or 10,000 U/ml of the Th1-associated cytokine interferon-beta, for 24 hr, after which RNA was isolated for evaluation by quantitative PCR and protein was collected for Western blot analysis. RESULTS: HLA-G5 but not G1 was present in dAEC as demonstrated by quantitative PCR, western blot and confocal microscopy. Neither G5 nor G1 expression was increased by the Th2-associated cytokines IL-4, IL-5 or IL-13 over 24 hr, nor after treatment with IL-10, but was increased 4.5 +/- 1.4 fold after treatment with 10,000 U/ml interferon-beta. CONCLUSIONS: These data demonstrate the constitutive expression of a T lymphocyte regulatory molecule in differentiated human airway epithelial cells that is not modulated by Th2-associated cytokines. FAU - White, Steven R AU - White SR AD - University of Chicago, Section of Pulmonary and Critical Care Medicine, Chicago, IL 60637, USA. swhite@medicine.bsd.uchicago.edu FAU - Loisel, Dagan A AU - Loisel DA FAU - Stern, Randi AU - Stern R FAU - Laxman, Bharathi AU - Laxman B FAU - Floreth, Timothy AU - Floreth T FAU - Marroquin, Bertha A AU - Marroquin BA LA - eng GR - HL-095268/HL/NHLBI NIH HHS/United States GR - HL-072414/HL/NHLBI NIH HHS/United States GR - HL-080417/HL/NHLBI NIH HHS/United States GR - U19 AI095230/AI/NIAID NIH HHS/United States GR - AI-056352/AI/NIAID NIH HHS/United States GR - AI-095320/AI/NIAID NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20130118 PL - England TA - Respir Res JT - Respiratory research JID - 101090633 RN - 0 (Cytokines) RN - 0 (HLA-G Antigens) SB - IM MH - Cell Differentiation MH - Cells, Cultured MH - Cytokines/*immunology MH - Epithelial Cells/*cytology/*immunology MH - HLA-G Antigens/*immunology MH - Humans MH - Immunomodulation/*immunology MH - Respiratory Mucosa/cytology/*immunology MH - Th2 Cells/*immunology PMC - PMC3560103 EDAT- 2013/01/19 06:00 MHDA- 2013/07/13 06:00 PMCR- 2013/01/18 CRDT- 2013/01/19 06:00 PHST- 2012/10/03 00:00 [received] PHST- 2013/01/11 00:00 [accepted] PHST- 2013/01/19 06:00 [entrez] PHST- 2013/01/19 06:00 [pubmed] PHST- 2013/07/13 06:00 [medline] PHST- 2013/01/18 00:00 [pmc-release] AID - 1465-9921-14-4 [pii] AID - 10.1186/1465-9921-14-4 [doi] PST - epublish SO - Respir Res. 2013 Jan 18;14(1):4. doi: 10.1186/1465-9921-14-4.