Th1 CD4+Cells Adoptively Transfer Experimental Hypersensitivity Pneumonitis

Schuyler, Mark; Gott, Katherine; Cherne, Amy; Edwards, Bruce S.

doi:10.1006/cimm.1997.1107

Cited by 75 publications

(53 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, when the Th1/Th2 balance shift toward a Th1 response, the HP is more severe, while it is attenuated by Th2-biased immune responses (9 -12). Moreover, in a murine model, the adoptive transfer of Th1 clones induced reversible HP (13,14). These observations suggest that the development of HP in animal models is determined by the modulation of Th1/Th2 immune responses in vivo.…”

Section: Il-4-secreting Nkt Cells Prevent Hypersensitivitymentioning

confidence: 77%

IL-4-Secreting NKT Cells Prevent Hypersensitivity Pneumonitis by Suppressing IFN-γ-Producing Neutrophils

Hwang

Kim

Park

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

Hypersensitivity pneumonitis (HP) is mediated by Th1 immune response. NKT cells regulate immune responses by modulating the Th1/Th2 balance. Therefore, we postulated that NKT cells play a critical role in the development of the HP by modulating the Th1/Th2 response. To address this issue, we explored the functional roles of NKT cells in Saccharopolyspora rectivirgula (SR)-induced HP. In CD1d−/− mice, the HP was worse in terms of histological changes, hydroxyproline levels, the CD4:CD8 ratio in bronchoalveolar lavage fluid, and SR-specific immune responses than in control mice. CD1d−/− mice showed elevated IFN-γ production in the lung during the HP, and this was produced mainly by Gr-1+ neutrophils. The blockade of IFN-γ in CD1d−/− mice attenuated the HP, whereas the injection of rIFN-γ aggravated it. Moreover, the depletion of Gr-1+ neutrophils reduced CD8+ T cell numbers in bronchoalveolar lavage fluid during the HP. The adoptive transfer of IL-4−/− mouse NKT cells did not attenuate the HP, whereas wild-type or IFN-γ−/− mouse NKT cells suppressed the HP. In conclusion, NKT cells producing IL-4 play a protective role in SR-induced HP by suppressing IFN-γ-producing neutrophils, which induce the activation and proliferation of CD8+ T cells in the lung.

show abstract

Section: Il-4-secreting Nkt Cells Prevent Hypersensitivitymentioning

confidence: 77%

IL-4-Secreting NKT Cells Prevent Hypersensitivity Pneumonitis by Suppressing IFN-γ-Producing Neutrophils

Hwang

Kim

Park

et al. 2006

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…T cells play a critical role in the development of granulomas in HP; athymic nude mice that lack T cells develop a significantly less severe form of HP following SR exposure compared to their normal counterparts [5]. In addition, CD4 + T cells from SR-exposed donors can adoptively transfer sensitization to naive recipients [6,7]. The T cell lines that adoptively transferred disease were characterized as Th1 cells, since they produced high levels of the Th1 cytokine IFN-c and no IL-4.…”

Section: Introductionmentioning

confidence: 99%

IFN-γ production by innate immune cells is sufficient for development of hypersensitivity pneumonitis

Nance

Cross

et al. 2005

Eur. J. Immunol.

View full text Add to dashboard Cite

“…Athymic nude mice that lack T cells develop a significantly less severe form of HP following SR exposure compared to normal mice [9]. Finally, CD4 + T cells from SR-exposed mice can adoptively transfer sensitization to naive recipients [10,11]. The T cell lines that adoptively transferred disease were characterized as Th1 cells since they produced high levels of the Th1 cytokine IFN-+ and low levels of the Th2 cytokine IL-4.…”

Section: Introductionmentioning

confidence: 99%

Chemokine production during hypersensitivity pneumonitis

2004

View full text Add to dashboard Cite

Hypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to inhaled particulate antigens. Individuals with HP develop lymphocytic alveolitis, granuloma formation, and fibrosis. HP is categorized as a Th1 disease, and granuloma formation is dependent on T cells and the Th1 cytokine IFN-+ . We therefore hypothesized that the IFN-+ -inducible chemokines IP-10, Mig, and I-TAC, which are frequently associated with Th1 diseases, would play an important role in the pathogenesis of disease. We analyzed the expression of multiple chemokines in the lungs of wild-type (WT) and IFN-+ -knockout (GKO) mice exposed to the particulate antigen Saccharopolyspora rectivirgula (SR). Our results demonstrate the production of IP-10, Mig, and I-TAC in WT mice during the development of HP, whereas GKO mice have reduced levels of IP-10 and no Mig or I-TAC mRNA in the lungs in response to SR exposure. The production of these chemokines is associated with an influx of CXCR3 + /CD4 + T cells into lungs of WT mice, which is reduced in GKO mice. These results suggest that IFN-+ mediates the recruitment of CXCR3 + /CD4 + T cells into the lung via production of the chemokines IP-10, Mig, and I-TAC, resulting in granuloma formation.

show abstract

Th1 CD4+Cells Adoptively Transfer Experimental Hypersensitivity Pneumonitis

Cited by 75 publications

References 44 publications

IL-4-Secreting NKT Cells Prevent Hypersensitivity Pneumonitis by Suppressing IFN-γ-Producing Neutrophils

IL-4-Secreting NKT Cells Prevent Hypersensitivity Pneumonitis by Suppressing IFN-γ-Producing Neutrophils

IFN-γ production by innate immune cells is sufficient for development of hypersensitivity pneumonitis

Chemokine production during hypersensitivity pneumonitis

Contact Info

Product

Resources

About