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Table II

Cure of Leishmaniasis after GK1.5-based Immunotherapy Is Associated with Unipolar Th1-type Cytokine Responses

GroupAntigen-induced cytokine levels
IFN-γIL-4*
  ng/ml ± SEM 
Experiment 1     
 Control (n = 5)  1.42 ± 0.19  1.24 ± 0.35 
 Immunotherapy (n = 5)  0.88 ± 0.39  0.06 ± 0.02 
Experiment 2     
 Uninfected  0.11  ≤0.05 
 Control (n = 5)  1.36 ± 0.07  1.28 ± 0.17 
 Immunotherapy (n = 3)  1.01 ± 0.12  0.05 
 Nonhealing (n = 2)§  2.08  1.53 
GroupAntigen-induced cytokine levels
IFN-γIL-4*
  ng/ml ± SEM 
Experiment 1     
 Control (n = 5)  1.42 ± 0.19  1.24 ± 0.35 
 Immunotherapy (n = 5)  0.88 ± 0.39  0.06 ± 0.02 
Experiment 2     
 Uninfected  0.11  ≤0.05 
 Control (n = 5)  1.36 ± 0.07  1.28 ± 0.17 
 Immunotherapy (n = 3)  1.01 ± 0.12  0.05 
 Nonhealing (n = 2)§  2.08  1.53 

BALB/c mice were treated with GK1.5 and 11B11 mAb, followed by intralesional rIL-12 as described in the text. Lymph node cells were harvested after disease recovery at wk 4 of reinfection (Experiment 1) or at wk 7 after immunotherapy (Experiment 2) and were cultured for 48 h in the presence of 10 μg/ml of soluble leishmania antigen. Cytokine concentrations were measured by specific ELISA. Control lymph node cells were from BALB/c mice infected for 4 wk with L. major.  

*

 IL-4 was measured in antigen-stimulated cultures to which anti–IL-4 receptor mAb had been added (10 μg/ml). IL-4 levels in all cultures were reduced by >96% in the presence of anti–MHC II mAb.  

 Antigen-stimulated IFN-γ production was reduced 60.8 ± 5.4% for control mice and 46.3 ± 7.5% for immunotherapy mice after neutralization of MHC II by anti–I-Ed/I-Ad mAb added at 10 μg/ml to antigen-stimulated cultures.  

§

Two mice failed therapy, as indicated by chronic footpad swelling and cutaneous ulceration.  

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