Nonbilayer Phospholipid Arrangements Are Toll-Like Receptor-2/6 and TLR-4 Agonists and Trigger Inflammation in a Mouse Model Resembling Human Lupus

Table 1

Gene expression in mice with a disease resembling human lupus triggered by liposomes with Mn²⁺-induced or chlorpromazine-induced nonbilayer phospholipid arrangements.

	Genes
Pathways with overexpression of genes
Complement system	Classical pathway: C1ra, C1s, C1q, C3, C5, and C7
	Receptors of the classical pathway: C3ar1 and C5ar1
	Alternative pathway: Cfd, Cfh, and Cfhr2
Exogenous antigen presentation	H2-aa, H-2aa, H2-dma, and Clip
Antibody production	Igh-vj558, Lyn, Syk, Plcg2, Can, Akt1, and Nfkb1
TLR-4 signalling	Tlr-4, Tram, Trif, Tbk1, Irf3, Ifn-α, and Ifn-β
NOD-2 signalling	Nod-2, Ripk2, Card9, Mapk10, and Tnfa
Pathways with underexpression of genes
Apoptosis	Casp8, Cycs, Apaf1, and Aifm1
Recognition of NK cells	Klrb1a, Klrb1c, Klra23, Klra7, Gzmb, and Klra22

Genes that were over- or underexpressed in mice injected with Mn-induced nonbilayer phospholipid arrangements (Mn group) or chlorpromazine-induced nonbilayer phospholipid arrangements (CPZ group), compared with mice injected with liposomes without nonbilayer phospholipid arrangements (Control II). The cutoff for over- and underexpressed genes was set as mean fold change log₂ ratio greater than +2 or lower than −2, as assessed by two-way ANOVA, with p < 0.01.