PMID- 16785543
OWN - NLM
STAT- MEDLINE
DCOM- 20060809
LR  - 20200914
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 177
IP  - 1
DP  - 2006 Jul 1
TI  - Pneumocystis cell wall beta-glucans induce dendritic cell costimulatory molecule 
      expression and inflammatory activation through a Fas-Fas ligand mechanism.
PG  - 459-67
AB  - Respiratory failure during Pneumocystis pneumonia is mainly a consequence of 
      exaggerated inflammatory responses to the organism. Dendritic cells (DCs) are the 
      most potent APCs in the lung and are key to the regulation of innate and adaptive 
      immune responses. However, their participation in the inflammatory response 
      directed against Pneumocystis infection has not been fully elucidated. Therefore, 
      we studied the role of Pneumocystis carinii, as well as Saccharomyces cerevisiae, 
      cell wall-derived beta-glucans, in DC costimulatory molecule expression. We 
      further studied the impact of beta-glucans on subsequent T cell activation. 
      Because cytokine secretion by DCs has recently been shown to be regulated by Fas 
      ligand (FasL), its role in beta-glucan activation of DCs was also investigated. 
      beta-Glucan-induced DC activation occurred in part through dectin-1 receptors. We 
      demonstrated that DC activation by beta-glucans elicits T cell activation and 
      polarization into a Th1 patterned response, but with the conspicuous absence of 
      IL-12. These observations differed from LPS-driven T cell polarization, 
      suggesting that beta-glucans and LPS signal DC activation through different 
      mechanisms. We additionally determined that IL-1beta and TNF-alpha secretion by 
      beta-glucan-stimulated DCs was partially regulated by Fas-FasL. This suggests 
      that dysregulation of FasL could further enhance exuberant and prolonged cytokine 
      production by DCs following DC-T cell interactions, further promoting lung 
      inflammation typical of Pneumocystis pneumonia.
FAU - Carmona, Eva M
AU  - Carmona EM
AD  - Thoracic Diseases Research Unit, Division of Pulmonary Critical Care and Internal 
      Medicine, Department of Medicine, Mayo Clinic College of Medicine, 200 First 
      Street SW, Rochester, MN 55905, USA.
FAU - Vassallo, Robert
AU  - Vassallo R
FAU - Vuk-Pavlovic, Zvezdana
AU  - Vuk-Pavlovic Z
FAU - Standing, Joseph E
AU  - Standing JE
FAU - Kottom, Theodore J
AU  - Kottom TJ
FAU - Limper, Andrew H
AU  - Limper AH
LA  - eng
GR  - R01 HL062150/HL/NHLBI NIH HHS/United States
GR  - HL 62150/HL/NHLBI NIH HHS/United States
GR  - R01 HL 55934/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Cytokines)
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Faslg protein, rat)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Ligands)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Tumor Necrosis Factor Inhibitors)
RN  - 0 (Tumor Necrosis Factors)
RN  - 0 (beta-Glucans)
RN  - 0 (beta-glucan receptor)
RN  - 0 (dectin 1)
RN  - 0 (fas Receptor)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Animals
MH  - Binding, Competitive/immunology
MH  - Cell Proliferation
MH  - Cell Wall/chemistry/*immunology
MH  - Coculture Techniques
MH  - Cytokines/antagonists & inhibitors/biosynthesis/metabolism
MH  - Dendritic Cells/*immunology/*metabolism/pathology
MH  - Down-Regulation/immunology
MH  - Fas Ligand Protein
MH  - Humans
MH  - Inflammation Mediators/antagonists & inhibitors/metabolism/*physiology
MH  - Interleukin-12/deficiency/metabolism
MH  - Lectins, C-Type
MH  - Ligands
MH  - Membrane Glycoproteins/antagonists & inhibitors/metabolism/*physiology
MH  - Membrane Proteins/metabolism/physiology
MH  - Nerve Tissue Proteins/metabolism/physiology
MH  - Pneumocystis/chemistry/*immunology
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptors, Immunologic/metabolism/physiology
MH  - Saccharomyces cerevisiae/immunology
MH  - T-Lymphocytes/cytology/immunology
MH  - Tumor Necrosis Factor Inhibitors
MH  - Tumor Necrosis Factors/metabolism/*physiology
MH  - beta-Glucans/*immunology/metabolism
MH  - fas Receptor/metabolism/*physiology
EDAT- 2006/06/21 09:00
MHDA- 2006/08/10 09:00
CRDT- 2006/06/21 09:00
PHST- 2006/06/21 09:00 [pubmed]
PHST- 2006/08/10 09:00 [medline]
PHST- 2006/06/21 09:00 [entrez]
AID - 177/1/459 [pii]
AID - 10.4049/jimmunol.177.1.459 [doi]
PST - ppublish
SO  - J Immunol. 2006 Jul 1;177(1):459-67. doi: 10.4049/jimmunol.177.1.459.