| First Author | Dent AL | Year | 1999 |
| Journal | J Immunol | Volume | 163 |
| Issue | 4 | Pages | 2098-103 |
| PubMed ID | 10438949 | Mgi Jnum | J:56751 |
| Mgi Id | MGI:1342381 | Doi | 10.4049/jimmunol.163.4.2098 |
| Citation | Dent AL, et al. (1999) BCL-6-deficient mice reveal an IL-4-independent, STAT6-dependent pathway that controls susceptibility to infection by Leishmania major. J Immunol 163(4):2098-103 |
| abstractText | The BCL-6 gene negatively regulates Th2 responses as shown by the finding that BCL-6-deficient (BCL-6-/-) mice develop a lethal Th2-type inflammatory disease. The response of inbred mouse strains to infection with Leishmania major is under genetic control; BALB/c mice are susceptible and develop a progressive parasite burden, whereas most other common laboratory strains of mice are resistant to infection. We found that BCL-6-/- mice on a resistant genetic background (C57BL/6 x 129 intercrossed mice) were highly susceptible to L. major infection; they resembled BALB/c mice in terms of lesion size, parasite load, and the production of Th2 cytokines. BCL-6-/-IL-4-/- double-mutant mice were also susceptible to L. major infection and produced 10-fold higher levels of the Th2 cytokine IL-13 than IL-4-/- littermate controls. By contrast, BCL-6-/-STAT6-/- double-mutant mice were resistant to L. major infection despite also producing elevated levels of IL-13. These results show that STAT6 is required for susceptibility to L. major infection and suggest that IL-13 signaling through STAT6 may contribute to a nonhealing, exacerbated L. major infection. |
