| First Author | Kusunoki T | Year | 2003 |
| Journal | J Allergy Clin Immunol | Volume | 111 |
| Issue | 1 | Pages | 136-42 |
| PubMed ID | 12532109 | Mgi Jnum | J:105840 |
| Mgi Id | MGI:3616749 | Doi | 10.1067/mai.2003.29 |
| Citation | Kusunoki T, et al. (2003) TH2 dominance and defective development of a CD8+ dendritic cell subset in Id2-deficient mice. J Allergy Clin Immunol 111(1):136-42 |
| abstractText | BACKGROUND: Although the TH1/TH2 balance is important in many clinical situations, the regulatory mechanisms in vivo have not been well elucidated. OBJECTIVE: We sought to characterize the immunologic status of mice lacking Id2, an inhibitor of basic helix-loop-helix transcription factors. METHODS: We analyzed serum immunoglobulin levels, gene-expression profiles in the spleen, TH1/TH2 balance, and dendritic cell (DC) populations of Id2-/- mice. RESULTS: Serum levels of TH2-mediated IgG1 and IgE were increased more than 10-fold in Id2-/- mice without antigenic stimulation. Gene-expression analysis in Id2-/- splenocytes revealed enhanced expression of TH2-related genes, such as IL-4, and reduced expression of TH1-related genes, including IFN-gamma and IL-12. Intracellular cytokine staining also confirmed that Id2-/- splenic CD4+ T cells are substantially skewed to TH2 cells. However, Id2-/- naive CD4+ T cells differentiated into TH1 cells comparably with wild-type T cells under the appropriate culture conditions. Id2-/- mice displayed a selective and remarkable reduction of the CD8+ DC subset, which is known to induce preferential TH1 differentiation.CONCLUSION: Id2 is an indispensable regulator of the TH1/TH2 balance, possibly through the proper development of CD8alpha+ DCs, and could be a novel target to treat allergic diseases. |
