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. 2005 Jun;140(3):478–490. doi: 10.1111/j.1365-2249.2005.02779.x

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© 2005 British Society for Immunology

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Fig. 5 — Serum IgA (10 mg/ml) induced modulation of the release of chemokines: monocyte chemoattractant protein 1 (MCP1), macrophage inflammatory protein 1 alpha (MIP1α) and beta (MIP1β). The results are arithmetic means from triplicate cultures ± SD (n = 3) stimulated for 24 h (representative results from one blood donor). Monocytes and PBMC were stimulated with LPS alone (), or with LPS in the presence of serum IgA: Lot 582 () or Lot 593 (). To estimate the influence of IgA on resting monocytes or on resting PBMC the cells were incubated with IgA alone: Lot 582 () or Lot 593 (▪). Control cells were cultured in medium (Med) alone (□). Statistically significant difference between either IgA-treated versus control cultures or IgA + LPS-treated versus LPS alone denoted as: *P < 0·05, **P < 0·01, ***P < 0·001.

Inline graphic — Serum IgA (10 mg/ml) induced modulation of the release of chemokines: monocyte chemoattractant protein 1 (MCP1), macrophage inflammatory protein 1 alpha (MIP1α) and beta (MIP1β). The results are arithmetic means from triplicate cultures ± SD (n = 3) stimulated for 24 h (representative results from one blood donor). Monocytes and PBMC were stimulated with LPS alone (), or with LPS in the presence of serum IgA: Lot 582 () or Lot 593 (). To estimate the influence of IgA on resting monocytes or on resting PBMC the cells were incubated with IgA alone: Lot 582 () or Lot 593 (▪). Control cells were cultured in medium (Med) alone (□). Statistically significant difference between either IgA-treated versus control cultures or IgA + LPS-treated versus LPS alone denoted as: *P < 0·05, **P < 0·01, ***P < 0·001.