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B7‐DC‐expressing Dendritic Cells Sequentially Promote and Limit Th1, Th2, and Th17 Responses in Lung‐draining Lymph Nodes
Author(s) -
Oriss Timothy B.,
Krishnamoorthy Nandini,
DixonMcCarthy Barbara,
Arora Meenakshi,
Zheng Mingquan,
Kolls Jay K.,
Ray Prabir,
Ray Anuradha
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.663.17
Subject(s) - immune system , dendritic cell , immunology , t cell , inflammation , cytokine , lung , biology , myeloid , microbiology and biotechnology , chemistry , medicine
Under conditions that result in inflammation of the airways, increased expression of the “non‐conventional” co‐stimulatory molecule B7‐DC was observed on myeloid‐like dendritic cells (mDCs) in the lung‐draining lymph nodes. This enhanced B7‐DC expression was observed in murine models of airway inflammation which result in skewing towards Th1‐, Th2‐, and Th17‐biased responses and were generated using administration of OVA plus CpG ODN, OVA plus cholera toxin, or infection with Klebsiella pneumoniae, respectively. B7‐DC expression on mDCs early in the immune response was associated with enhanced T cell cytokine production whereas later in the immune response, mDCs expressing B7‐DC were less stimulatory than those lacking its expression. Inhibitory effects were at least partially mediated via T cell expression of PD‐1, the inhibitory ligand for B7‐DC, and stimulatory effects were assumed to occur through the presently unidentified co‐stimulatory ligand which has been proposed for B7‐DC. The results indicate that under Th1, Th2, as well as Th17 conditions, B7‐DC expression appears to promote T cell cytokine production early, but appears to participate in limiting chronic activation of cells in later stages of the immune response. This work was supported by NIH grants HL77430 to A.R., HL60207 to P.R., and an American Lung Association Dalsemer Award to T.O.