Journal
JOURNAL OF IMMUNOLOGY
Volume 177, Issue 7, Pages 4652-4661Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.7.4652
Keywords
-
Categories
Funding
- NHLBI NIH HHS [R01 HL 065912, R01 HL 051082] Funding Source: Medline
- NIAID NIH HHS [R01 AI 059201, R01 AI 049448, T32 AI 07413] Funding Source: Medline
Ask authors/readers for more resources
Maintenance of immunity to persistent pathogens is poorly understood. In this study, we used a murine model of persistent pulmonary fungal infection to study the ongoing cell-mediated immune response. CBA/J mice with low-level persistent Cryptococcus neoformans infection had CD4(+) T cells of effector memory phenotype present in their lungs. Although unable to eliminate the primary infection to sterility, these mice displayed hallmarks of immunologic memory in response to rechallenge with C. neoformans: 1) the secondary cryptococcal challenge was controlled much more rapidly, 2) the inflammatory response developed and resolved more rapidly, 3) CD4(+) T and CD8(+) T cell responses were higher in magnitude, and 4) effector cytokine production by T cells was greatly enhanced. Depletion of CD4(+) T cells at the time of secondary challenge adversely affected clearance of C. neoformans from the lungs. These results demonstrate that persistent low-level infection with C. neoformans does not impair the cell-mediated response to the fungus. Although they are relatively free of overt disease, these mice can respond with a rapid secondary immune response if the burden of C. neoformans increases. These data support the concept that immunologically healthy individuals can maintain low numbers of cryptococci that can become a nidus for re-activation disease during immunodeficient states such as AIDS.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available