Figure 8
Altered T-cell phenotype in IL-12/23 axis–deficient patients. (A) Circulating CD56+ T cells (top panel) and CD56− T cells (bottom panel) from indicated individuals were explored for their cell surface phenotype (except for perforin, where an intracytoplasmic staining was performed). Each dot indicates the value obtained from one individual. (B) Circulating CD56− T cells, CD56+ T cells, and NK cells from 4 representative healthy control individuals were assayed for their IFN-γ production in response to 24-hour treatment in the presence or absence of indicated cytokines: IL-2 (50 U/mL), IL-15 (10 ng/mL), IL-18 (20 ng/mL), IL-12 (5 ng/mL). (C) Circulating CD56− T cells, CD56+ T cells, and NK cells from 5 healthy individuals were assayed for their IFN-γ production in response to live BCG alone or BCG plus IL-12 (20 ng/mL) during 24 and 48 hours. Each line represents the response obtained with one individual.

Altered T-cell phenotype in IL-12/23 axis–deficient patients. (A) Circulating CD56+ T cells (top panel) and CD56 T cells (bottom panel) from indicated individuals were explored for their cell surface phenotype (except for perforin, where an intracytoplasmic staining was performed). Each dot indicates the value obtained from one individual. (B) Circulating CD56 T cells, CD56+ T cells, and NK cells from 4 representative healthy control individuals were assayed for their IFN-γ production in response to 24-hour treatment in the presence or absence of indicated cytokines: IL-2 (50 U/mL), IL-15 (10 ng/mL), IL-18 (20 ng/mL), IL-12 (5 ng/mL). (C) Circulating CD56 T cells, CD56+ T cells, and NK cells from 5 healthy individuals were assayed for their IFN-γ production in response to live BCG alone or BCG plus IL-12 (20 ng/mL) during 24 and 48 hours. Each line represents the response obtained with one individual.

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