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IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC–activated Th2 memory cells
The results provide a plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells.
A novel subset of CD4+ TH2 memory/effector cells that produce inflammatory IL-17 cytokine and promote the exacerbation of chronic allergic asthma
Memory CD4+ T cells that produce both Th2 and Th17 cytokines are increased in the blood of patients with atopic asthma and in the lungs of asthmatic mice, where they contribute to inflammation.
Pulmonary alveolar proteinosis caused by deletion of the GM-CSFRα gene in the X chromosome pseudoautosomal region 1
Using a combination of cellular, molecular, and genomic approaches, this work provides the first evidence that PAP can result from a genetic deficiency of the GM-CSFR α chain, encoded in the X-chromosome pseudoautosomal region 1.
Biology of common beta receptor-signaling cytokines: IL-3, IL-5, and GM-CSF.
Delineating the biology of these cytokines is enabling the development of new strategies for diagnosing and treating these diseases and modulating immune responses.
The biology of the immune system.
  • D. Huston
  • Biology, Medicine
  • 10 December 1997
This overview of the biology of theimmune system provides a framework for understanding physiologic immune responses and how lacunar defects within the immune system explain the pathogenesis of immunologic disorders.
CXCL13 neutralization reduces the severity of collagen-induced arthritis.
OBJECTIVE To investigate the role of CXCL13 in the development and pathogenesis of collagen-induced arthritis (CIA), and to determine the mechanisms involved in the modulation of arthritogenic
IL‐13 production by allergen‐stimulated T cells is increased in allergic disease and associated with IL‐5 but not IFN‐γ expression
It is concluded that allergen‐specific T’cells from atopic subjects secrete elevated quantities of IL‐13 compared with non‐atopic controls, in the context of a Th2‐type pattern of cytokine production.