Figure 3.
Inflammasome activation across different groups of patients presenting with KSHV-associated diseases stratified according to their clinical classification. (A) Plasma levels of IL-18 were compared among participants with KAD (n = 42, comprising patients with KS alone [10], MCD [11], MCD + PEL [5], KICS + KS [11], and PEL ± KS [5]; ∗means with or without KS), PWH (n = 12), and HV (n = 10). (B) PBMCs from the previously mentioned groups were incubated with the FLICA, and the gMFI of FLICA within total circulating blood monocytes was compared among groups. (C) Alternatively, PBMCs were also stained for monocyte identification and intracellular ASC and acquired by imaging flow cytometry. Data are presented as median with interquartile range. Data were analyzed using the Kruskal-Wallis test followed by Dunn multiple comparisons. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

Inflammasome activation across different groups of patients presenting with KSHV-associated diseases stratified according to their clinical classification. (A) Plasma levels of IL-18 were compared among participants with KAD (n = 42, comprising patients with KS alone [10], MCD [11], MCD + PEL [5], KICS + KS [11], and PEL ± KS [5]; ∗means with or without KS), PWH (n = 12), and HV (n = 10). (B) PBMCs from the previously mentioned groups were incubated with the FLICA, and the gMFI of FLICA within total circulating blood monocytes was compared among groups. (C) Alternatively, PBMCs were also stained for monocyte identification and intracellular ASC and acquired by imaging flow cytometry. Data are presented as median with interquartile range. Data were analyzed using the Kruskal-Wallis test followed by Dunn multiple comparisons. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

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