| First Author | Somigliana E | Year | 2001 |
| Journal | Fertil Steril | Volume | 75 |
| Issue | 1 | Pages | 203-6 |
| PubMed ID | 11163839 | Mgi Jnum | J:66996 |
| Mgi Id | MGI:1929584 | Doi | 10.1016/s0015-0282(00)01659-9 |
| Citation | Somigliana E, et al. (2001) Use of knockout transgenic mice in the study of endometriosis: insights from mice lacking beta(2)-microglobulin and interleukin-12p40. Fertil Steril 75(1):203-6 |
| abstractText | OBJECTIVE: To test the possibility of using transgenic knockout mice in the study of endometriosis and to investigate specific immunologic aspects of the disease. DESIGN: Experimental blinded study. SETTING: Academic research center. ANIMAL(S): Thirty-two mice with experimentally induced endometriosis. INTERVENTION(S): Endometriosis was induced in 8 beta(2)-microglobulin-deficient BALB/c mice and 7 wild-type BALB/c controls. Similarly, endometriosis was induced in 8 interleukin-12-deficient C57BL/6 mice and in 9 wild-type C57BL/6 controls. MAIN OUTCOME MEASURE(S): Weight and surface area of endometriotic lesions. RESULT(S): Total weight and surface area of endometriotic lesions was markedly lower in beta(2)-microglobulin-deficient BALB/c mice than in wild-type BALB/c controls. A slight but statistically insignificant increase in total weight and surface area of lesions was observed in interleukin-12-deficient C57BL/6 mice compared to wild-type C57BL/6 controls. CONCLUSION(S): Knockout transgenic mice can be used successfully for the study of endometriosis; however, in these animals, the redundancy of the immunologic cytokine-mediated regulatory mechanisms may lead to compensation from the remaining genome. Results from beta(2)-microglobulin-deficient mice support the critical role of the immune system in the pathogenesis of the disease. |
