Type-1 Interferon (IFN-1)

IFN-1 status is a prognostic factor for disease severity in SLE, including risk of progression to Lupus Nephritis. Many current and developmental therapeutics target IFN-1 along with TLR 7/8 receptors and the JAK/STAT signaling pathway.

Type-2 Interferon (IFN-γ)

IFN-γ plays a key role in T-cell differentiation, immunoregulatory, antiviral and anti-tumor activity. This 3-gene module is being evaluated for therapy response and disease activity in SLE, subtyping in RA, and immunotherapy response prediction in cancer.

B-Cell

Many common immunosuppressive therapies function through a B-cell depletion mechanism including recently approved Obinutuzumab, Rituximab, and Ocrevus. The B-cell module can be used to monitor therapeutic response for B-cell depleting therapies.

Plasmablast/Plasma Cell

This module has been shown to positively correlate with disease activity in SLE and is impacted by B-cell depleting therapies. Measuring these changes may aid clinicians in the early identification of changes in disease activity or potential disease flare.

Low Density Granulocytes (LDG) Neutrophils

Low density granulocytes are a subset of neutrophils that have been implicated in SLE systemic inflammation and disease progression, including kidney damage and progression to lupus nephritis.

T-Cells

The T-cell genes in MIP are looked at individually to help better understand the underlying mechanism of a patient’s autoimmune disease.

T-Cell Exhaustion

In chronic autoimmune disease like SLE, the process of T-cell exhaustion helps inhibit immune response, and exhausted T-cell responses have been associated with better outcomes. T-cell exhaustion mechanisms and markers also play a major role in cancer and how tumors hide from the immune system.