Human genomics is the study of human genetics with characteristics of wholeness,comprehensiveness and directivity. Although there is difference in the gene-guided protein synthesis among individual proteins, which requires to be validated by proteomic and cytological studies, comparisons of gene expression patterns among different groups and functional analysis of differentially expressed genes may provide a general view and a direction for the understanding of mechanisms underlying the pathogenesis of diseases. This is a unique feature of genomics and cannot be replaced by other methods.

Gene Ontology analysis of the gene expression in PE group targets the significant downregulations of T cell immune complexes and T cell immune functions when compared with the controls [17].

Phagocytes, NK cells, complement system and cytokine related gene expressions in both PE group and control group were compared.

mRNA expressions of pattern recognition receptors (TLR2, TLR4,CD14, MYD88, MRC1L1, MRC2, MSR1, SCARA5, SCARB2, SCARF1 and SCARF2) and opsonic receptors (CR1, FCGR2A, FCGR2B, FCGR3A and FCGR3B) were up-regulated in phagocytes of the PE group compared with controls, among which TLR4, CD14,MYD88, SCARB2, SCARF2, CR1 and FCGR2A were significantly up-regulated (P<0.001),indicating the increased functions of neutrophils and monocytes [18].

Compared with control group, NK cells related gene expressions declined overall in PE group, among which mRNA expressions of seven tenth of the lectin-like receptors and Natural cytotoxic receptors were significantly down-regulated(P<0.05), suggesting reduced functions of NK cells killing target cells directly [18].

There are 14 genes of complement early components. In PBMCs from PE patients, expression of the genes encoding C1qα, C1qβ, C4b and Factor P was significantly greater (P<0.01) than that in controls. Gene expression of MBL and MASP1 was lower (P<0.05) in PBMCs from PE patients compared with controls, and seven genes of the complement late components were detected. In PE patients, mRNA expression of C5 was significantly up-regulated (P<0.05), whereas C6, C7 and C9 were significantly down-regulated (P<0.05) compared with controls. In PE patients, expression levels of all the seven genes mRNAs were up-regulated, and mRNA expressions of CR1,integrin αM, integrin αX and C5aR were significantly up-regulated (P b 0.01) compared with controls. Gene expressions of complement regulators C4b binding protein, α(C4BPα), C4b binding protein, β (C4BPβ), Factor H, Factor I, CD59, CD55 and CD46 in PBMCs from PE patients and controls were detected. CD59 and CD55 mRNAs were both significantly up-regulated (P<0.05), while Factor I mRNA was significantly downregulated (P<0.05) in PBMCs from PE patients than controls, and the other 3 genes showed down-regulated trend. mRNA expression of various components, receptors and regulators of the complement pathways were unbalanced in PE patients, indicating the interruption of complement system cascade reactions and the loss of complement mediated membrane attacking functions [19].

In PBMCs from PE patients, the expression levels of genes encoding IFNα5,IFNα6, IFNα8, IFNα14, IFNκ, IFNω1 and IFNε1 were significantly lower than those detected in PBMCs from controls (P<0.05). IFNγ mRNA expression was significantly downregulated in PBMCs from PE patients compared with controls (P<0.01) [20].

A total of 37 interleukin genes were detected. In comparison with the control, the expression levels of 12 genes were downregulated specifically IL1A,IL9, IL17B, IL19, IL23A and IL25 (P<0.05), IL2, IL3, IL13, IL22, IL24 and IL31 (P<0.01),and those of two of the genes, IL10 and IL28A, were upregulated (P<0.05), in the PE patients. The imbalance of Th1/Th2 manifests as reduced cell-mediated immunity [20,21].

Twelve genes encoding CXC chemokines were detected. In PE patients, mRNA expression levels of Cxcl1, Cxcl2, Cxcl6, Cxcl13 and Cxcl14 were significantly upregulated (P<0.05), and Cxcl10 mRNA expression levels were significantly downregulated compared with controls (P<0.01). Twenty-three genes encoding CC chemokines were examined and the mRNA expression levels of CC chemokines were significantly lower in PE patients than controls (P<0.01) [20].

Thirty-eight genes encoding members of the TNF superfamily and TNF receptor superfamily were examined. In PE patients, the mRNA expression levels of TNF superfamily members 1, 9 and 13, and TNF receptor superfamily members 1A, 1B,9, 10B, 10C, 10D and 19L, were significantly upregulated (P<0.05), whereas TNF receptor superfamily members 11B, 19 and 25, were significantly downregulated compared with controls (P<0.05) [20].

Six genes encoding colony stimulating factors were detected and the mRNA expression levels of granulocyte-macrophage colony stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF),erythropoietin (EPO), thrombopoietin (THPO) and mast cell growth factor (KITLG)were significantly lower in PBMCs from PE patients than controls (P<0.05) [20].

Eight genes associated with transforming growth factor(TGF), epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF)were detected. The mRNA expression levels of TGFβ1, TGFβ1-induced transcript 1,EGF and VEGF were significantly upregulated (P<0.01), whereas TGFβ3 mRNA was significantly downregulated (P<0.05) in PBMCs from PE patients compared with controls [20].

From the characteristics of a variety of cytokine mRNA expression levels in PE patients, we conclude that the immune function and the ability of clearing viruses,intracellular bacteria and parasites are reduced in PE patients [20].

In patients with PE, the expression of the majority of integrin mRNAs located on leukocytes and platelets was significantly upregulated. The expression of mRNAs related to L-selectin and P-selectin glycoprotein ligand was significantly upregulated,while the expression of mRNA related to E-selectin was significantly downregulated.The expression of mRNAs related to classic cadherins and protocadherins was downregulated, and the expression of mRNAs related to vascular endothelial cadherin was significantly downregulated; the expression of mRNAs related to the immunoglobulin superfamily had no obvious difference between the 2 groups.In conclusion, we demonstrated that, in symptomatic PE patients, the adhesion of leukocytes and platelets was enhanced; the activation of endothelial cells was obviously weakened; the adherens junctions among endothelial cells were weakened, with the endothelium becoming more permeable [22].

Among the 13 leukocyte-related integrin mRNAs, integrins β1 and β2 mRNAs expressions were upregulated in the PE group, compared with the controls (P<0.05). Of the 7 platelet-related integrin mRNAs, integrins β2 and β3 mRNAs expressions were upregulated in the PE group, compared with the controls (P<0.05). Among the 11 other integrin mRNAs, 6 were upregulated (of which 3 significantly) in the PE group (P<0.05)and 5 were downregulated (of which 3 significantly) (P<0.01). It can be concluded that most leukocyte- and platelet- related integrin mRNAs were upregulated in the PE group, as well as fibronectin- and fibrinogen- related integrin mRNAs [22].

T and B lymphocyte related gene expressions in both PE group and control group were compared.

Of the 6 genes of T cell immunological synapse, receptor complex, plasmalemma and receptors mRNAs, ZAP70, CD247 and GZMB mRNAs were downregulated in the PE group, compared with the controls (P<0.05), while GZMA,CD3G and CD3D mRNAs downregulated in the PE group, compared with the controls(P<0.01) [18].

mRNA expressions of 82 genes involved in B cell activation were detected.(i)B cell receptor: In PE patients, expressions of LYN, CD22, SYK, BTK, PTPRC and NFAM1 were signif i cantly higher, whereas expressions of FYN, FCRL4 and LAX1 were significantly lower than the control group. (ii)T cell dependent B cell activation:In PE patients, mRNA expressions of EMR2, TNFSF9, CD86, ICOSLG, CD37 and CD97 were signif i cantly up-regulated, whereas SPN mRNA was signif i cantly downregulated compared with the control group. (iii)T cell independent B cell activation:LILRA1 and TLR9 mRNAs were signif i cantly up-regulated in PE patients compared with the control group. (iv)Regulators: In PE patients, expressions of the genes including CR1, LILRB4 and VAV1 were signif i cantly higher, whereas expression of SLAMF7 was signif i cantly lower than those in the control group. (v) Cytokines: In PE patients, expressions of genes including LTA and IL10 were signif i cantly higher,whereas expressions of L1A, IFNA5, IFNA6, IFNA8, IFNA14, IL2, IL13 and IFNG were signif i cantly lower than those in the control group. It is indicated that Deferential gene expressions in dif f erent stages of B cell activation suggest the decrease or disorders of B cell function [23].

The whole genomics results showed significantly decreased functions of T lymphocytes, disorganized functions of B lymphocytes and complements, and inflammations with enhanced immune adherence.