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. 2022 Aug 24;13:953439. doi: 10.3389/fimmu.2022.953439

Table 3.

Overlaps of disease networks supporting Figures 3 (Murine T1D, Lupus, Peripheral and Central tolerance) and Figure 6 (all 8 networks combined).

Network Overlaps in Figure 3 Overlaps in Figure 6
Exp. Overlapsa Fold O-Rb Pc Exp. Overlapsa Fold O-Rb Pc
Monogenic SLE X X X 0.92 18 1.5E-17
Polygenic SLE X X X 2.17 15 1.5E-28
Monogenic T1D X X X 0.14 22 2.6E-04
Polygenic T1D X X X 1.19 16 4.3E-18
murine lupus 0.58 26 1.9E-17 1.57 16 1.9E-23
murine T1D 0.13 32 6.8E-06 0.34 26 1.6E-11
peripherald 0.14 86 1.5E-21 0.38 51 2.2E-31
centrald 0.04 45 8.2E-04 0.12 17 5.8E-03

Overlap of disease networks supporting Figures 3 (Murine T1D, Lupus, Peripheral and Central tolerance) and Figure 6 (all 8 networks combined). aExp. Overlaps indicate the number of expected overlapping nodes. Assuming similar length lists were randomly selected from the genome (unassociated). bFold O-R indicates the fold over-representation compared to expectation. cP indicates p-value for hypergeometric distribution assuming independence of the two networks. dperipheral and central indicate networks of genes implicated in peripheral and central B cell tolerance. As a negative control, comparison was made to the L2G predicted causal genes in a large GWAS of osteoarthritis (452) and type 2 diabetes (453). In both cases, overlap was substantially less than in the table above. A single putative causal gene out of 19 for osteoarthritis overlapped with the network in Figure 6. This corresponds to 3-fold overrepresentation with P-value of 0.27. 17 putative causal gene out of 343 for type 2 diabetes overlapped with the network in Figure 6. This corresponds to 2.9-fold overrepresentation with P-value of 9E-5. Of note, the overlapping genes were enriched for genes within apoptosis and cellular proliferation pathways. As these core cellular processes impact both the genesis of autoimmune pathology and insulin resistance, this degree of overlap is perhaps not surprising.