This article reviews a selection of presentations at the 2010 annual meeting of the European Respiratory Society held in Barcelona, Spain, which was the largest congress ever in the field of respiratory medicine. The best abstracts from the groups of the Clinical Assembly (Clinical Problems, Rehabilitation and Chronic Care, Imaging, Interventional Pulmonology, Diffuse Parenchymal Lung Disease, and General Practice and Primary Care) are presented in the context of the current literature.
Ifngr1-/- mice develop more severe experimental autoimmune encephalomyelitis (EAE) with delayed onset compared to wild-type (WT) mice. Enhanced disease severity in Ifngr1-/- mice was associated with elevated numbers of both Th1 and Th17 cells in the central nervous system. Elevated Th17 population was expected, but the expanded numbers of Th1 cells in Ifngr1-/- mice contradicts the paradigm that IFNγ signaling is a positive feedback loop for Th1 expansion. Furthermore, cultures of encephalitogenic T cells isolated from these mice restimulated under Th1 skewing conditions contained several fold greater numbers of IFNγ-expressing Th cells than WT T cell cultures. These observations led us to investigate the possibility that IFNγ participates in a negative feedback loop associated with Th1 differentiation. Addition of suboptimal levels of neutralizing anti-IFNγ mAb during in vitro polarization of encephalitogenic WT T cells to Th1 cells led to at least a two-fold greater number of CD4+IFNγ+ T cells. Suboptimal neutralization of IFNγ didn’t alter the generation and/or expansion of Th1 cells when encephalitogenic T cells were obtained from Ifngr1-/- or Stat1-/- mice, confirming the requirement for intact IFNγ signaling. Contrary to the traditional dogma, these data suggest that IFNγ can negatively regulate Th1 differentiation, which may partly explain the opposing biology of IFNγ in EAE and multiple sclerosis.
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