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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: Expert Rev Clin Immunol. 2011 Sep;7(5):611–626. doi: 10.1586/eci.11.53

Figure 1. Current understanding of the cross-talk between endometrial cells, peritoneal (mesothelial) cells and multiple immune cells via proinflammatory chemokines/cytokines.

Figure 1

Dysregulation of cell-mediated immunity in endometriosis, compared to disease-free women with no clinical evidence of endometriosis, accounts for the survival and growth of endometriotic tissue. Specifically, nonapoptotic menstrual debris escapes detection and elimination by immune cells, initiating an inflammatory cascade via production of chemokines/cytokines.

ENA-78: Epithelial cell-derived neutrophil-activating peptide 78; KIR: Killer-cell immunoglobulin-like receptor; LFA1: Lymphocyte function-associated antigen 1; MCP-1: Monocyte chemotactic protein-1; MMP-9: Matrix metalloproteinase-9; NK: Natural killer; PGE2: Prostaglandin E2; sICAM-1: Soluble ICAM-1.