Alan P Knutsen, Clifford Bellone, Henk Kauffman 

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Immunopathogenesis of allergic bronchopulmonary aspergillosis in cystic fibrosis  Alan P Knutsen, Clifford Bellone, Henk Kauffman  Journal of Cystic Fibrosis  Volume 1, Issue 2, Pages 76-89 (June 2002) DOI: 10.1016/S1569-1993(02)00033-4

Fig. 1 Model of pathogenesis of allergic bronchopulmonary aspergillosis (from Knutsen et al. [1]). Journal of Cystic Fibrosis 2002 1, 76-89DOI: (10.1016/S1569-1993(02)00033-4)

Fig. 2 Asp f1-specific T-cell line was rested for 2–17 days after IL-2 and Asp f1 stimulation (top panel). Supernatant IL-4 concentration was measured serially. Significant amounts of IL-4 were synthesized for up to 10–14 days of rest. Monoclonal anti-IL-4 antibody inhibited Asp f1-stimulated lymphoproliferation of antigen-specific T-cell lines in a dose–response manner (bottom panel). Maximum inhibition was 84% at 5% anti-IL-4 antibody concentration (v/v) in this experiment and 78% in a second experiment. Anti-IL-2 had little inhibition of proliferation, indicating an IL-4-dependent autocrine lymphoproliferative response (from Knutsen et al. [34]). Journal of Cystic Fibrosis 2002 1, 76-89DOI: (10.1016/S1569-1993(02)00033-4)

Fig. 3 IL-4 induction of CD23+ molecules on CD20+ and on CD86+ CD20+ B-cells. ABPA CF patients had significantly increased number of CD23 molecules (a) per B-cell and (b) per CD86+ B-cell on day 0 compared to non-ABPA CF patients (P<0.01) and non-atopic control patients (P<0.01). Following IL-4 stimulation, ABPA CF patients had a significantly increased rate of CD23+ expression (a) per B-cell and (b) per CD86+ B-cell compared to non-ABPA CF (P<0.01) and non-atopic control patients (P<0.01). Data presented as mean±S.E. (from Knutsen et al. [66]). Journal of Cystic Fibrosis 2002 1, 76-89DOI: (10.1016/S1569-1993(02)00033-4)

Fig. 4 IL-13 induction of CD23+ molecules on CD20+ and on CD86+ CD20+ B-cells. Following IL-13 stimulation, ABPA CF patients had no significantly increased rate of CD23+ expression (a) per B-cell and (b0 per CD86+ B-cell compared to non-ABPA CF and non-atopic control patients (P<0.01). Data presented as mean±S.E. (from Knutsen et al. [66]). Journal of Cystic Fibrosis 2002 1, 76-89DOI: (10.1016/S1569-1993(02)00033-4)

Fig. 5 Th1 and Th2 CD3+ T cells. (a) Following PMA and ionomycin stimulation, ABPA CF patients had comparable percentages of IFN-γ and IL-4 CD3+ T-cells compared to non-ABPA CF patients. However, both ABPA and non-ABPA CF patients had significantly decreased percentages of IFN-γ CD3+ T-cells compared to normal control subjects (P<0.001, P<0.001 respectively). (b) Following tetanus toxoid and Asp f2/3/4 stimulation, both ABPA and non-ABPA CF patients had significantly decreased IFN-γ CD3+ T-cells compared to normal control subjects (P<0.05, P<0.05, respectively) but not different from each other. However, ABPA CF patients had significantly increased Asp f2/3/4-stimulated IL-4 CD3+ T-cells compared to non-ABPA CF patients and normal control subjects (P<0.01, P<0.01, respectively). Data presented as mean±S.E. (from Knutsen et al. [66]). Journal of Cystic Fibrosis 2002 1, 76-89DOI: (10.1016/S1569-1993(02)00033-4)