| First Author | Allen HL | Year | 2006 |
| Journal | J Immunol | Volume | 177 |
| Issue | 3 | Pages | 1763-71 |
| PubMed ID | 16849486 | Mgi Jnum | J:138028 |
| Mgi Id | MGI:3803564 | Doi | 10.4049/jimmunol.177.3.1763 |
| Citation | Allen HL, et al. (2006) B cells and CD4-CD8- T cells are key regulators of the severity of reactivation histoplasmosis. J Immunol 177(3):1763-71 |
| abstractText | The fungus, Histoplasma capsulatum, produces a persistent infection. Reactivation histoplasmosis is largely a result of impaired immunity, but the perturbations associated with escape of the fungus from host defenses remain ill-defined. We analyzed a murine model of reactivation to elucidate the host defects that permit reactivation. C57BL/6 mice were infected intranasally and, 42 days later, they were depleted of CD4(+) and CD8(+) cells. Elimination of these cells, but not either alone, produced a persistent infection over several weeks. Neutralization of IFN-gamma, TNF-alpha, or both did not induce reactivation. Endogenous IL-10 exacerbated reactivation. Depletion of T cells in B cell(-/-) mice induced a markedly higher burden in organs when compared with wild type. However, the infection remained persistent. Elimination of CD4(+) cells alone or neutralization of cytokines increased the fungal load. The persistent infection was not dependent on gammadelta T cells or NK cells. Elimination of Thy-1.2(+) cells in mice given mAb to CD4 and CD8 transformed reactivation into a progressive, lethal infection in B cell(-/-) and wild-type mice, but the tempo of progression was accelerated in the former. The data reveal the complex control by the host to prevent reactivation of this fungus. |
