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Table 1
Potential biomarkers and their proposed applications in SLE
Category	Biomarker	Associations	Comments

Susceptibility	IRF-5
	STAT-4 HLA-DRB1	Specific haplotypes confer increased susceptibility to SLE. Genome-wide association studies have identified many loci, mostly related to immune	Genetic epistasis between different loci has been described
	PTPN22	regulatory genes
	Fcγ receptors
	Complement proteins	Deficiency in early components of the classical complement pathway is a strong risk factor for SLE	Partial C4 deficiency due to gene copy number variations increases the risk of SLE
Disease activity	IFNα	High levels of IFNα or IFN inducible genes	Despite the association with activity, the
		(IFN signature) and chemokines correlated with disease activity	IFN signature was not predictive of flare in longitudinal studies
	B-cell subsets	CD27^highplasma cells correlated with disease activity
	Serum cytokines, receptors and adhesion molecules	Multiple cytokines (for example, IL-6, IL-10, IL-16, IL-18), soluble receptors (sIL-2 R) and adhesion molecules (for example, sICAM and sVCAM) have been suggested to correlate with disease activity	Data are limited and almost all proposed candidates are still far from being established as a reliable marker in SLE
Disease severity	IFNα	High IFN signature group has more severe disease manifestations	Holds the potential to identify high-risk patients
Disease subtype	IFNα	High versus low IFN groups have distinct clinical features, autoantibody associations and genetic profiles	IFN signature and BLyS levels may potentially define subgroups of patients
	BLyS	High BLyS levels are associated with specific autoantibodies
Flares	BLyS	Higher and rising BLyS levels were predictive of increase in disease activity at subsequent visit	The association has not been consistent across the studies
Organ specific	Anti-C1-q antibodies	Correlate with the presence and severity of lupus nephritis	Potential robust marker for lupus nephritis
	Anti-NR2 antibodies	Associated with neuropsychiatric manifestations in a murine model	Human results have been largely negative

Anti NR2 antibodies, anti-N-methyl-D-asparate (NMDA) receptor antibodies; BLyS, B-lymphocyte stimulator; HLA, human leukocyte antigen; IFN, interferon; IRF, interferon regulatory factor; PTPN22, protein tyrosine phosphatase N22; sICAM, soluble intracellular adhesion molecule; SLE, systemic lupus erythematosus; STAT, signal transduction and activator of transcription; sVCAM, soluble vascular adhesion molecule.
Lateef and Petri Arthritis Research & Therapy 2012 14(Suppl 4):S4 doi:10.1186/ar3919

Table 1