ELISA

Cathepsin S, also known as CTSS, is a protein that in humans is encoded by the CTSS gene. A member of the peptidase C1 family, CTSS gene is a lysosomal cysteine proteinase that may participate in the degradation of antigenic proteins to peptides for presentation on MHC class II molecules. By fluorescence in situ hybridization(FISH), this gene is mapped to 1q21.3. The encoded protein can function as an elastase over a broad pH range in alveolar macrophages. The bond-specificity of this proteinase is in part similar to the specificities of cathepsin L and cathepsin N.

Insulin-like growth factor-binding protein 6(IGFBP6) is a protein that in humans is encoded by the IGFBP6 gene. The IGFBP6 gene is mapped to chromosome 12. In all, it has contained 216 amino acid protein with a calculated molecular mass of 22,847, The human keratinocyte cell line HaCat secretes IGFBP6 as an autocrine growth inhibitor. Recombinant IGFBP6 was also shown to inhibit growth of HaCat cells and other keratinocyte cell lines.

MHC class I polypeptide-related sequence B, also called MICB is a protein that in humans is encoded by the MICB gene. The MICB gene is mapped to 6p21.33. This gene encodes a heavily glycosylated protein which is a ligand for the NKG2D type II receptor. Binding of the ligand activates the cytolytic response of natural killer(NK) cells, CD8 alphabeta T cells, and gammadelta T cells which express the receptor. This protein is stress-induced and is similar to MHC class I molecules; however, it does not associate with beta-2-microglobulin or bind peptides. It seems to have no role in antigen presentation. This gene acts as a stress-induced self-antigen that is recognized by gamma delta T cells. It is the ligand for the KLRK1/NKG2D receptor and binds to KLRK1 leads to cell lysis.

Interferon lambda-1, also called Interleukin-29(IL-29) is a protein that in humans is encoded by the IL29 gene. IL-29 is a member of the helical cytokine family and is a type III interferon. This gene is mapped to 19q13.2. It is a cytokine with immunomodulatory activity. This gene may play a role in antiviral immunity. It can up-regulates MHC class I antigen expression. It is the ligand for the heterodimeric class II cytokine receptor composed of IL10RB and IFNLR1. The ligand/receptor complex seems to signal through the Jak-STAT pathway. IL-29 plays an important role in host defenses against microbes and its gene is highly upregulated in cells infected with viruses.

Follistatin-related protein 1, also called FSTL1 or FRP is a protein that in humans is encoded by the FSTL1 gene. FSTL1 gene is mapped to chromosome 3q13.33 based on an alignment of FSTL1 sequence with the genomic sequence(GRCh37). This gene encodes a protein with similarity to follistatin, an activin-binding protein. It contains an FS module, a follistatin-like sequence containing 10 conserved cysteine residues. This gene product is thought to be an autoantigen associated with rheumatoid arthritis. This gene may modulate the action of some growth factors on cell proliferation and differentiation. It was suggested that fibroblast-secreted FSTL1 acts on macrophages to increase TNF and IL1B production and IL6 activity.

C5a is a protein fragment released from complement component C5. This gene is mapped to 9q33.2. The protein encoded by this gene is the fifth component of complement, which plays an important role in inflammatory and cell killing processes. This protein is comprised of alpha and beta polypeptide chains that are linked by a disulfide bridge. An activation peptide, C5a, which is an anaphylatoxin that possesses potent spasmogenic and chemotactic activity, is derived from the alpha polypeptide via cleavage with a convertase. The C5b macromolecular cleavage product can form a complex with the C6 complement component, and this complex is the basis for formation of the membrane attack complex, which includes additional complement components. Mutations in this gene cause complement component 5 deficiency, a disease where patients show a propensity for severe recurrent infections. Defects in this gene have also been linked to susceptibility to liver fibrosis and to rheumatoid arthritis.

Extracellular link domain containing 1, also known as LYVE-1 or XLKD1 is a human gene. The International Radiation Hybrid Mapping Consortium mapped the LYVE1 gene to chromosome 11p15.4. This gene encodes a type I integral membrane glycoprotein. The encoded protein acts as a receptor and binds to both soluble and immobilized hyaluronan. This protein may function in lymphatic hyaluronan transport and have a role in tumor metastasis. This gene may play a role in autocrine regulation of cell growth mediated by growth regulators containing cell surface retention sequence binding(CRS). It may act as a hyaluronan(HA) transporter, either mediating its uptake for catabolism within lymphatic endothelial cells themselves, or its transport into the lumen of afferent lymphatic vessels for subsequent re-uptake and degradation in lymph nodes.

Interferon lambda-2, also called IFNL2 or IL28A is a class II cytokine receptor ligand related to type I interferons. This gene is mapped to 19q13.2. This gene encodes a cytokine distantly related to type I interferons and the IL-10 family. This gene, interleukin 28B(IL28B), and interleukin 29(IL29) are three closely related cytokine genes that form a cytokine gene cluster. It up-regulates MHC class I antigen expression. It also displays antitumor activity. The ligand/receptor complex seems to signal through the Jak-STAT pathway. This gene seems not to be essential for early virus-activated host defense in vaginal infection, but plays an important role in Toll-like receptor(TLR)-induced antiviral defense. It seems play a significant role in the antiviral immune defense in the intestinal epithelium.

RAGE, the Receptor for Advanced Glycation Endproducts, is a 35kD transmembrane receptor of the immunoglobulin super family. It is also known as “AGER”. AGER gene is mapped to chromosome 6p21.3 by mapping by contiguous cosmids and YAC clones and by fluorescence in situ hybridization. The expression of RAGE is particularly increased in neurons close to deposits of amyloid beta peptide and to neurofibrillary tangles. RAGE has been linked to several chronic diseases, which are thought to result from vascular damage. The pathogenesis is hypothesized to include ligand binding upon which RAGE signals activation of the nuclear factor kappa B(NF-kappaB).