Table 1. Genes of different co-expression patterns in pathology compared with health donors as displayed by mosaics of correlations in Figure 4.

Order on Figure 4/symbol/name	References and description
4/ETS2/V-ets erythroblastosis virus E26 oncogene homolog 2	(3) There was an increased expression of ets-2 in 30% of rheumatoid arthritis samples and an up to 30-fold decreased expression of the potential metastasis suppressor gene nm23-H1 in 90% of RA tissues, compared with control tissues.
	(4) demonstrated a role for the ETS1 and ETS2 transcription factors in regulating the expression of p16(INK4A) in these different contexts based on their ability to activate the p16(INK4A) promoter through an ETS binding site and their patterns of expression during the life span of human diploid fibroblasts.
	(5) They studied the expression of cyclin-dependent kinase inhibitors in rheumatoid synovial cells as a means of suppressing synovial cell proliferation. Synovial cells derived from hypertrophic synovial tissue readily expressed p16INK4a when they were growth-inhibited. This was not seen in other fibroblasts, including those derived from normal and osteoarthritis-affected synovial tissues. In vivo adenoviral gene therapy with the p16INK4a gene efficiently inhibited the pathology in an animal model of rheumatoid arthritis. Thus, the induction of p16INK4a may provide a new approach to the effective treatment of rheumatoid arthritis.
6/JUNB/Jun B proto-oncogene	(6) Differential junB mRNA expression in synovial membranes and isolated synovial fibroblasts from rheumatoid arthritis patients
20/TIAF1/TGFB1-induced anti-apoptotic factor 1	(7) TGFB1-induced anti-apoptotic factor 1 inhibits tumor necrosis factor cytotoxicity.
	(8) TIAF1 binds to Jak3 and inhibits apoptosis induced by IL-2 deprival.
	(9) TIAF1 protects murine L929 fibroblasts from TNF cytotoxicity. TIAF1 induced growth inhibition and apoptosis of monocytic U937 and other types of cells. TIAF1 increased the expression of p53, Cip1/p21, and Smad proteins; suppressed ERK phosphorylation; and altered TGF-beta1-mediated Smad2/3 phosphorylation in U937 cells. Antisense TIAF1 mRNA significantly enhanced the proliferation of mink lung Mv1Lu epithelial cells. Together, these observations indicate that TIAF1 participates in the TGF-beta-mediated growth regulation.
	(10) T helper cells are important modulators of the allograft immune response. A small number of genes are already known to be differentially expressed in T helper 1 (Th1) and T helper 2 (Th2) cells, but it is likely that many other genes are functionally important. To study gene expression in Th1 and Th2 cells, we used serial analysis of gene expression. One of the differentially expressed genes was TIAF-1, which is a TGF-beta 1-induced antiapoptotic factor, known to inhibit the cytotoxic effects of tumor necrosis factor-alpha on mouse fibroblasts. We hypothesized that TIAF-1 differentially expressed in Th1 and Th2 cells and plays a protective role against apoptosis during allograft rejection.
	TIAF-1 mRNA and protein were not detectable in normal kidney and liver; however, the expression of TIAF-1 was up-regulated in most biopsy specimens with chronic and a few with acute allograft rejection. Immunohistochemistry for TIAF-1 revealed expression in the inflammatory infiltrate and in tubular epithelialcells. CONCLUSIONS: TIAF-1 mRNA and protein are predominantly up-regulated in kidney and liver allografts with chronic rejection. Expression of TIAF-1 in the lymphocytes during chronic allograft rejection may be related to the predominance of a Th2 response in this condition. The expression in the transplanted tissue may protect these cells from apoptosis.
21/STAT6/signal transducer and activator of transcription 6, interleukin-4 induced	(11) CD23 is atypically highly expressed in various chronic diseases, including B-CLL, lupus erythematodes and rheumatoid arthritis. Cooperation between NF-AT and STAT factors might be one of the molecular mechanisms responsible for high-level expression of CD23 on the surface of B-CLL cells.
	(12) Serum soluble CD23 levels and CD23 expression on peripheral blood mononuclear cells in juvenile chronic arthritis.
	(13) The finding that STAT6(−/−) T(h)2 cells did not show any down-regulation of VLA-2 expression and expressed the same levels of VLA-2 as T(h)1 cells indicated a critical role for the IL-4 receptor/STAT6 signaling pathway in IL-4-dependent down-regulation of VLA-2 on T(h)2 cells. Our results indicate that VLA-2 is a novel functional marker that dissociates T(h)1 from T(h)2 cells, and thus might be useful for therapeutic monitoring of T(h)1-dependent immune diseases such as rheumatoid arthritis or Crohn's disease.
27/WARS/tryptophanyl-tRNA synthetase	(14) Sera of patients bearing autoimmune diseases (rheumatoid arthritis and systemic lupus erythematosus) show the presence of autoantibodies against tryptophanyl-, tyrosyl- and phenylalanyl-tRNA synthetases.
28/BMP2/bone morpho-genetic protein 2	(15) Bone morphogenetic proteins 2 and 6, expressed in arthritic synovium, are regulated by proinflammatory cytokines and differentially modulate fibroblast-like synoviocyte apoptosis.