Acquired predisposition to mycobacterial disease due to autoantibodies to IFN-γ
J. Clin. Invest. Beate Kampmann, et al. 115:2480 doi:10.1172/JCI19316 [Go to this article.]

Figure 4
High-density cDNA microarrays showing functional activity of IFN-γ–binding antibody. PBMCs from a healthy donor were exposed to 4 different conditions — no treatment with IFN-γ or antibody (control); IFN-γ alone; IFN-γ with the patient antibody (pt Ab); and IFN-γ with a nonspecific antibody (ns Ab) — each over 4 time points (0, 2, 6, and 21 hours). After data selection and normalization, we filtered for genes demonstrating at least 2.5-fold change from baseline at any 2 of the time points surveyed. The resulting genes were ordered by agglomerative hierarchical clustering (average linkage method) using Cluster software. The genes are displayed in rows, time points in columns. Induced genes are depicted in red, repressed genes in green. Gray represents missing data. When the patient’s purified anti–IFN-γ antibody was present with IFN-γ, the gene expression profile most closely resembled that of the control subject. Cluster I shows TNF genes; cluster II, genes most affected by the presence of the antibody; and cluster III, expression of IFN-γ.