Y Yoshida’s research while affiliated with Case Western Reserve University and other places

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Publications (7)

FIG. 1. IL-10 and IL-12 production by monocytes treated with live C. albi- cans SC5341 or live C. krusei 6258. Human PBMC were treated with live C. albicans SC5314 (L- CA SC5314 ) or C. krusei 6258 (L- CK 6258 ). Supernatants were collected after incubation for 20 h. Cytokines were measured by ELISA. Monocytes without fungal cells were used as controls (C). n ϭ 18 for IL-10; n ϭ 16 for IL-12; ء , P Ͻ 0.05 versus control; ءء , P , Ͻ 0.01 versus control. 
FIG. 2. Expression of IL-12 p40 mRNA in human peripheral blood monocytes was inhibited by C. albicans species. Human peripheral blood monocytes were cocultured with live C. albicans SC5314, 1442, 2307, and 2183 (L-CA SC5314, L-CA 1442, L-CA 2183, and L-CA 2307, respectively), C. krusei 6258 and A-L (L-CK 6258 and L-CK A-L, respectively), or monocytes alone as control for 20 h. Total RNA was extracted, and RT-PCR was conducted with primers for IL-12 p40 and-actin. Results are representative of two separate experiments that yielded similar results.
Live Candida albicans, but not Candida krusei, selectively fails to induce human blood mononuclear cells IL-12 and IFN-Y production
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May 2000

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Infection and Immunity

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Kang K

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Liu L

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Protection against Candida infection involves both innate and acquired immune responses, and cytokines produced by monocytes during the innate response may modify the acquired immune response by T cells. We hypothesized that Candida species which differ in pathogenicity can differentially induce production of immunoregulatory cytokines by human monocytes, which in turn modify T cells for immune responses to Candida. To test this hypothesis, we examined the effects of Candida albicans and Candida krusei on immunoregulatory cytokine production by human monocytes and gamma interferon (IFN-gamma) production by peripheral blood mononuclear cells (PBMC). Purified monocytes were incubated with live or heat-killed strains of C. albicans and C. krusei at the optimal Candida/monocyte ratio of 0.5. Cytokines in the supernatants were measured by enzyme-linked immunosorbent assay. Our data demonstrated that live C. albicans and C. krusei significantly induced interleukin-10 (IL-10), monocyte chemotactic factor 1, IL-1beta, and tumor necrosis factor alpha production by monocytes relative to unstimulated monocytes. In contrast, unlike C. krusei, pathogenic live strains of C. albicans induced no or only a minimal level of IL-12. The expression of IL-12 p40 mRNA levels by reverse transcription-PCR corroborated the IL-12 protein (p70) findings. In human PBMC, human blood monocytes were the major source of both IL-10 and IL-12 production in response to C. albicans and C. krusei. Upon activation of T cells in the presence of Candida-modified monocytes and antigen-presenting cells, IL-12 production by PBMC treated with Candida organisms correlated strongly with the level of IFN-gamma production by T cells. These results indicate that the virulence of C. albicans may be related to its ability to induce the monocytic type II cytokine IL-10, with a selective inhibition of IL-12 production, which may be responsible for the observed lack of T-cell IFN-gamma and may restrain an effective type I immune response to Candida.

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