Table 4.
KEGG pathways overrepresented in matched vs mismatched MLC regulated genesa
| Pathways | Count | % | P‐value | Benjamini |
|---|---|---|---|---|
| Cytokine–cytokine receptor interaction | 17 | 1.4 | 7.6E‐9 | 5.5E‐7 |
| Toll‐like receptor signalling pathway | 8 | 0.7 | 9.2E‐5 | 3.3E‐3 |
| Chemokine signalling pathway | 10 | 0.8 | 1.5E‐4 | 3.6E‐3 |
| Haematopoietic cell lineage | 7 | 0.6 | 2.9E‐4 | 5.3E‐3 |
| Graft‐vs‐host disease | 5 | 0.4 | 7.6E‐4 | 1.1E‐2 |
| Type I diabetes mellitus | 5 | 0.4 | 1.0E‐3 | 1.2E‐2 |
| NOD‐like receptor signalling pathway | 5 | 0.4 | 4.3E‐3 | 4.3E‐2 |
| Antigen processing and presentation | 5 | 0.4 | 1.2E‐2 | 1.0E‐1 |
| JAK‐STAT signalling pathway | 6 | 0.5 | 2.5E‐2 | 1.8E‐1 |
MLC, mixed lymphocyte culture.
a
KEGG pathways found to be significantly overrepresented within differentially regulated genes between matched and mismatched MLC. Gene set enrichment analysis was performed using the molecular signatures database of DAVID Bioinformatics Resources (National Institute of Allergy and Infectious Diseases, National Institutes of Health). P values are corrected using Benjamini multiple testing correction and a cut‐off of P < 0.05.