Figure 1
Anticryptococcal activity of IL-2–activated PBLs was due to CD4+ T cells. PBLs were cultured with or without IL-2 for 7 days and activated PBLs were depleted of CD4+ T cells, CD8+ T cells, or NK cells by magnetic separation. C neoformans was incubated with PBLs at different E/T ratios or PBLs depleted of CD4+ T cells (CD4(−)), CD8+ T cells (CD8(−)), or NK cells (NK(−)) for 24 or 48 hours. The number of C neoformans (CFU) was determined in each group. Results are expressed as mean ± SEM. *P < .05 compared with the inoculum; #P < .01 compared with the number of C neoformans alone at 24 or 48 hours; ‡P < .05 compared with the number of C neoformans in the presence of IL-2–stimulated PBLs; NS, no significant difference, compared with the number of C neoformans in the presence of IL-2–stimulated PBLs. Data are representative of 2 independent experiments.

Anticryptococcal activity of IL-2–activated PBLs was due to CD4+ T cells. PBLs were cultured with or without IL-2 for 7 days and activated PBLs were depleted of CD4+ T cells, CD8+ T cells, or NK cells by magnetic separation. C neoformans was incubated with PBLs at different E/T ratios or PBLs depleted of CD4+ T cells (CD4(−)), CD8+ T cells (CD8(−)), or NK cells (NK(−)) for 24 or 48 hours. The number of C neoformans (CFU) was determined in each group. Results are expressed as mean ± SEM. *P < .05 compared with the inoculum; #P < .01 compared with the number of C neoformans alone at 24 or 48 hours; ‡P < .05 compared with the number of C neoformans in the presence of IL-2–stimulated PBLs; NS, no significant difference, compared with the number of C neoformans in the presence of IL-2–stimulated PBLs. Data are representative of 2 independent experiments.

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