Figure 5
Figure 5. T lymphocytes control the severity of innate inflammatory responses. (A) Cytokine production in vitro by male and female resident peritoneal cells (2 × 105 cells/sample, n = 6 mice) after 3 hours of stimulation by TLR4-specific LPS (0.1 μg/mL) or the TLR2 agonist Pam3CSK4 (Pam3, 0.1μg/mL). (B) TNFα production by isolated resident male peritoneal macrophages (1.5 × 105 cells/sample, n = 3 mice) treated with LPS (0.1μg/mL, 18 hours) in the absence or presence of CD4+ T lymphocytes (1.5 × 105 cells). (C) Zymosan-induced (1 mg IP for 3 hours) recruitment of GR1+ granulocytes into the peritoneal cavity of C57BL/6 (wild-type) and T-lymphocyte–deficient Rag2 knockout (KO) mice (n = 5 mice). All values are expressed as means ± SEM. #P < .05 by 1-way ANOVA compared with male; §P < .05 by 1-way ANOVA relative to macrophages alone; and *P < .05 by Student t test relative to wild-type.

T lymphocytes control the severity of innate inflammatory responses. (A) Cytokine production in vitro by male and female resident peritoneal cells (2 × 105 cells/sample, n = 6 mice) after 3 hours of stimulation by TLR4-specific LPS (0.1 μg/mL) or the TLR2 agonist Pam3CSK4 (Pam3, 0.1μg/mL). (B) TNFα production by isolated resident male peritoneal macrophages (1.5 × 105 cells/sample, n = 3 mice) treated with LPS (0.1μg/mL, 18 hours) in the absence or presence of CD4+ T lymphocytes (1.5 × 105 cells). (C) Zymosan-induced (1 mg IP for 3 hours) recruitment of GR1+ granulocytes into the peritoneal cavity of C57BL/6 (wild-type) and T-lymphocyte–deficient Rag2 knockout (KO) mice (n = 5 mice). All values are expressed as means ± SEM. #P < .05 by 1-way ANOVA compared with male; §P < .05 by 1-way ANOVA relative to macrophages alone; and *P < .05 by Student t test relative to wild-type.

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