Dependent allergic asthma model

Yet, whether l,25(OH)2D3 is an inducer of Th2 T cell responses remains controversial because l,25(OH)2D3 may also suppress IL-4 if present during the process of in vitro polarization of naive CD62L+ CD4+ T cells [130]. This may explain why 1,25 (OH)2D3 does not exclusively inhibit Thl-mediated diseases but also has beneficial effects in a Th2-dependent allergic asthma model (our own unpublished data). Moreover, l,25(OH)2D3 and its analog EB1089 are potent suppressors of IgE secretion from B cells activated with anti-CD40 and IL-4 [39]. Also, Thl, Th2 as well as ThO T cells are clearly susceptible to l,25(OH)2D3, since it inhibits phorbol myristate acetate (PMA)/ionomycin-induced proliferation of all three types of purified CD4+ T cells [38],... 

Janssen EM. van Oosterhout AJ, van Rensen AJ. van Eden W. Nijkamp FP. Wauben MH Modulation of Th2 responses by peptide analogues in a murine model of allergic asthma amelioration or deterioration of the disease process depends on the Thl or Th2 skewing characteristics of the therapeutic peptide. J Immunol 2000 164 580-588. 

Herz U, Ruckert R, Wollenhaupt K, Tschernig T, Neuhaus-Steinmetz U, Pabst R, Renz H Airway exposure to bacterial superantigen (SEB) induces lymphocyte-dependent airway inflammation associated with increased airway responsiveness - a model for non-allergic asthma. Eur J Immunol 1999 29 1021-1031. 

To better understand the pathogenesis of human asthma, a variety of experimental approaches using murine models of allergic pulmonary inflammation have been developed. In murine models of human asthma, it is apparent that initiation of the allergic immune response is T-lymphocyte dependent (1,2). However, the predominant direct mediator(s) of allergic inflammation identified in these murine... 

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