| First Author | Stamm LM | Year | 1998 |
| Journal | J Immunol | Volume | 161 |
| Issue | 11 | Pages | 6180-8 |
| PubMed ID | 9834104 | Mgi Jnum | J:51096 |
| Mgi Id | MGI:1314585 | Doi | 10.4049/jimmunol.161.11.6180 |
| Citation | Stamm LM, et al. (1998) Mice with STAT6-targeted gene disruption develop a Th1 response and control cutaneous leishmaniasis. J Immunol 161(11):6180-8 |
| abstractText | The cutaneous growth of Leishmania mexicana was measured in STAT6-deficient mice (STAT6-/-) and compared with that in similarly infected wild-type (STAT6+/+) mice. Following s.c. inoculation with 5 x 10(6) amastigotes of L. mexicana into the shaven rump, STAT6+/+ mice developed large, nonhealing cutaneous lesions, while STAT6-/- mice failed to develop detectable lesions during most of the course of study. As infection progressed, STAT6+/+ mice infected with L. mexicana displayed significantly higher titers of Leishmania-specific IgG1 and IgE compared with STAT6-/- mice, which conversely produced significantly higher titers of Leishmania-specific IgG2a, indicating development of a Th1-like response in the latter group. At 12 wk postinfection, Leishmania Ag-stimulated lymph node cells from STAT6-/-mice produced significantly higher amounts of IL-12 and IFN-gamma than those from STAT6+/+ mice as measured by ELISA. However, there was no significant difference in IL-4 production between the two groups. Semiquantitative RT-PCR of transcript levels in intact draining lymph nodes and skin from inoculation sites confirmed a similar pattern of cytokines in vivo as that observed in stimulated lymph node cells in vitro. These results indicate that STAT6-mediated IL-4 signaling is critical for progression of L. mexicana infection in genetically susceptible mice and demonstrate that in the absence of STAT6, susceptible mice default toward a Th1-like response and control cutaneous L. mexicana infection. |
