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Cellular nucleic acid-binding protein (CNBP) is a nucleic-acid binding protein with seven zinc-finger domains, which has a preference for binding single stranded DNA and RNA. CNBP serves in cap-independent translation of ornithine decarboxylase mRNA, and also in sterol-mediated transcriptional regulation. The expansion of A CCTG in CNBP protein’s first intron results in myotonic dystrophy type 2.

GDNF Family Receptor Alpha 3 (GFRA3) belongs to the GDNF receptor family. GFRA3 creates a signaling receptor complex with RET tyrosine kinase receptor and binds the ligand, artemin (ARTN).

TNFR1 belongs to the TNF-receptor superfamily. TNFR1 is a receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha.
There are 2 types of soluble TNF receptors: sTNFR-I and sTNFR-II, which act to neutralize the biological activities of TNF alpha and TNF beta. The levels of these soluble receptors seem to increase as a result of shedding of the extracellular domains of the membrane bound receptors. TNF-a, TNFR1 and TNFR2 have roles in cellular differentiation. TNFR1 and TNFR2 function in cell type-specific renal injury.
TNFR1 is capable of signaling both cell survival and apoptosis. TNFR1-induced apoptosis requires 2 sequential signaling complexes. TNFR1 is capable of activating NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Oxidative stress promotes TNFR1 and TNFR2 self-interaction, ligand-independent and enhanced ligand-dependent TNF signaling. TNFR1 contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase. Human TNFR1 has a major region which controls cell surface expression. High levels of soluble TNF receptors are found in the amniotic fluid of pregnant women.
Germline mutations of the extracellular domains of TNFR1 are linked to the autosomal dominant periodic fever syndrome. The impaired receptor clearance is believed to be a mechanism of the disease. Familial hibernian fever (FHF) is caused by defects in TNFRSF1A gene.

GZMK is a part of a group of related serine proteases from the cytoplasmic granules of cytotoxic lymphocytes. Cytolytic T lymphocytes and natural killer cells have the outstanding ability to bind, recognize and lyse specific target cells. They defend their host by lysing cells bearing on their surface 'nonself' antigens, usually peptides or proteins resulting from infection by intracellular pathogens.

VZV is closely related to the herpes simplex viruses(HSV), sharing much genomehomology. The known envelope glycoproteins (gB, gC, gE, gH, gI, gK, gL) correspond with those in HSV, however there is no equivalent of HSV gD. VZV virons are spherical and 150-200 nm in diameter. Their lipidenvelope encloses the nucleocapsid of 162 capsomeres arranged in a hexagonalform. Its DNAis a single, linear, double-stranded molecule, 125,000 nt long. The virus is very susceptible to disinfectants, notably sodium hypochlorite. Within the body it can be treated by a number of drugs and therapeutic agents including aciclovir, zoster-immune globulin(ZIG), and vidarabine.

Hepatitis A Virus Cellular Receptor 2 (HAVCR2) is a member of the immunoglobulin superfamily. HACVR2 controls macrophage activation. HACVR2 inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and stimulates immunological tolerance.

Low affinity immunoglobulin gamma Fc region receptor III-A (FCGR3A) is a receptor for the Fc portion of immunoglobulin G, and is involved in the elimination of antigen-antibody complexes from the circulation, as well as other antibody-dependent responses. FCGR3A needs to associate with the gamma subunit of Fc epsilon. The FCGR3A receptor is expressed on natural killer (NK) cells as an integral membrane glycoprotein anchored through a transmembrane peptide, while FCGR3B is expressed on polymorphonuclear neutrophils (PMN) where the receptor is anchored through a phosphatidylinositol (PI) linkage. In addition, FCGR3A is expressed on macrophages, subpopulation of T-cells, immature thymocytes and placental trophoblasts. FCGR3A mediates antibody-dependent cellular cytotoxicity (ADCC) and other antibody-dependent responses, such as phagocytosis. FCGR3A gene mutations are linked with susceptibility to recurrent viral infections, susceptibility to systemic lupus erythematosus, and alloimmune neonatal neutropenia.

IL2-Ra is one of the three constituent subunits of the IL2 receptor.
IL-2Ra is released into the serum after increased cellular expression such as increased activation of B and T cells. Clinical manifestations of IL2-Ra elevation include autoimmune conditions and some leukemias and lymphomas.

TNFR2 belongs to the TNF-receptor superfamily. TNFR2 is receptor with high affinity for TNFSF2/TNF-alpha and approximately 5-fold lower affinity for homotrimeric TNFSF1/lymphotoxin-alpha. TNFR2 mediates the majority of the metabolic effects of TNF-alpha. In addition, knockout studies in mice propose a role for TNFR2 in protecting neurons from apoptosis by stimulating antioxidative pathways. TNFR2 expression might have a significant role in the angiogenesis, tumor cell proliferation and metastasis of Invasive micropapillary carcinoma of the breast.
There are 2 types of soluble TNF receptors: sTNFR-I and sTNFR-II, which act to neutralize the biological activities of TNF alpha and TNF beta. The levels of these soluble receptors seem to increase as a result of shedding of the extracellular domains of the membrane bound receptors. High levels of soluble TNF receptors are found in the amniotic fluid of pregnant women. TNFR2 and TNFR1 form a heterocomplex which mediates the recruitment of 2 anti-apoptotic proteins, c-IAP1 and c-IAP2, which possess E3 ubiquitin ligase activity. IAPs’ function in TNF-receptor signaling is unknown; nevertheless, c-IAP1 is believed to potentiate TNF-induced apoptosis by the ubiquitination and degradation of TNF-receptor-associated factor 2, which mediates anti-apoptotic signals. Oxidative stress promotes TNFR1 and TNFR2 self-interaction, ligand-independent and enhanced ligand-dependent TNF signaling. TNF-a, TNFR1 and TNFR2 have roles in cellular differentiation. TNFR1 and TNFR2 function in cell type-specific renal injury.

Yersinia enterocolitica is a Gram-negative bacillus-shaped bacterium, which is a member of the Enterobacteriaceae family. Y.Enterocolitica is motile at temperatures between 22-29°C, however becomes non-motile at normal human body temperature. Y. Enterocolitica infection causes the yersiniosis disease, which is an animal-borne disease occurring in humans, as well as in a various groups of animals such as cattle, deer, pigs, and birds. Yersinia enterocolitica is a heterogeneous group of strains, which are conventionally classified by bio-typing into six bio-groups on the basis of phenotypic characteristics, and by serotyping into more than 57 “O” serogroups, on the basis of their O (lipopolysaccharide or LPS) surface antigen. Five of the six biogroups (1B and 2–5) are considered as pathogens. Nevertheless, only a few of these serogroups have been linked with disease in either humans or animals. Strains which belong to serogroups O:3 (biogroup 4), O:5,27 (biogroups 2 and 3), O:8 (biogroup 1B), and O:9 (biogroup 2) are most frequently isolated worldwide from human samples. Still, the main Y. enterocolitica serogroup in many European countries is serogroup O:3 followed by O:9, whereas the serogroup O:8 is mostly detected in the United States.

IL-29 is distantly related to type I interferons and the IL-10 family. Expression of IL-29 is induced by viral infection which interacts with a heterodimeric class II cytokine receptor that consists of interleukin 10 receptor, beta (IL10RB) and interleukin 28 receptor, alpha. IL-29 exhibits common features with type I IFNs such as antiviral activity, antiproliferative activity and in vivo antitumour activity.
IL-29 acts similarly to IFNs, but is less effective generally and has activity in a more limited range of cell lines. IFN-ambda 1, IFN-lambda 2 and IFN-lambda3 are closely positioned genes on human chromosome 19.
IL-29 induces ELR(-) CXC chemokine mRNA in human peripheral blood mononuclear cells, in an IFN-gamma-independent manner.
IL-29 is able to generate tolerogenic DCs, an activity that could thwart IFN-beta functions. IL-29 produced in response to viral infection, activates both monocytes and macrophages producing a restricted panel of cytokines and therefore is an important factor in activating innate immune responses at the site of viral infection.
IFN-Lambda 1 antiviral and antiproliferative activity requires Interferon-Lambda 2 receptor tyrosine residues.

Borrelia belongs to a genus of bacteria of the spirochete phylum. Borrelia causes borreliosis, which is a zoonotic, vector-borne disease transmitted mainly by ticks and some by lice, depending on the species. Of the 36 known species of Borrelia, 12 are distinguished to cause Lyme disease or borreliosis and are transmitted by ticks. The main Borrelia species causing Lyme disease are Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii. The Borrelia genus members have a linear chromosome which is about 900 kbp in length as well as an excess of both linear and circular plasmids in the 5-220 kbp size range. The plasmids are atypical, as compared to most bacterial plasmids, since they contain many paralogous sequences, a large number of pseudogenes and, in some cases, essential genes. Moreover, a number of the plasmids have features suggesting that they are prophages.

The protein encoded by this gene is a cytokine that acts as a growth and differentiation factor for both B cells and eosinophils. IL5is a main regulator of eosinopoiesis, eosinophil maturation and activation. The elevated production of IL5is reported to be related to asthma or hypereosinophilic syndromes. The receptor of IL5is a heterodimer, whose beta subunit is shared with the receptors for interleukine 3 (IL3) and colony stimulating factor 2 (CSF2/GM-CSF). IL5, together with those for interleukin 4 (IL4), interleukin 13 (IL13), and CSF2, form a cytokine gene cluster on chromosome 5. IL5, IL4, and IL13 are found to be regulated coordinately by long-range regulatory elements spread over 120 kilobases on chromosome 5q31.

Rat and mouse FGF-9 show a very high homology to human FGF-9. The transcripts for FGF-9 have been found in brain and in kidney tissue. Fibroblast Growth Factor-9 is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. FGF9 was isolated as a secreted factor that exhibits a growth-stimulating effect on cultured glial cells. In nervous system, this protein is produced mainly by neurons and may be important for glial cell development. Expression of the mouse homolog of this gene was found to be dependent on Sonic hedgehog (Shh) signaling. Mice lacking the homolog gene displayed a male-to-female sex reversal phenotype, which suggested a role in testicular embryogenesis Fibroblast Growth Factor 9 may have a role in glial cell growth and differentiation during development, gliosis during repair and regeneration of brain tissue after damage, differentiation and survival of neuronal cells, and growth stimulation of glial tumors.

Lymphotoxin alpha, a member of the tumor necrosis factor family, is a cytokine produced by lymphocytes. LTA is highly inducible, secreted, and exists as homotrimeric molecule. LTA forms heterotrimers with lymphotoxin-beta which anchors lymphotoxin-alpha to the cell surface. LTA mediates a large variety of inflammatory, immunostimulatory, and antiviral responses. LTA is also involved in the formation of secondary lymphoid organs during development and plays a role in apoptosis.

IL-12 is a heterodimeric cytokine that stimulates the production of interferon gamma from T-cells and natural killer cells, and also induces differentiation of Th1 helper cells. It is an initiator of cell-mediated immunity.

Tumor necrosis factor is a cytokine involved in systemic inflammation and is a member of a group of cytokines that all stimulate the acute phase reaction. TNF is mainly secreted by macrophages.
TNF causes apoptotic cell death, cellular proliferation, differentiation, inflammation, tumorigenesis and viral replication, TNF is also involved in lipid metabolism, and coagulation. TNF's primary role is in the regulation of immune cells.
Dysregulation and, in particular, overproduction of TNF have been implicated in a variety of human diseases- autoimmune diseases, insulin resistance, and cancer.

TRAIL Receptor-1 (DR4) and TRAIL Receptor-2(DR5) are members of the TNFR superfamily of transmembrane proteins and contain a cytoplasmic "death domain", which is capable of activating the cell's apoptotic machinery. These receptors are activated by binding to either membrane anchored or soluble TRAIL/Apo2L.

Zika virus (ZIKV) belongs to the family Flaviviridae and the genus Flavivirus, it is transmitted by daytime-active Aedes mosquitoes, such as A. aegypti and A. albopictus. The Zika virus is related to the dengue, yellow fever, Japanese encephalitis, and West Nile viruses. Much like the other flaviviruses, Zika virus is enveloped and icosahedral and has a nonsegmented, single-stranded, positive-sense RNA genome. Zika fever is an infection, which often causes no symptoms or only mild ones, like a mild form of dengue fever, and it is treated by rest. As of February 2016, there has been mounting evidence that Zika fever in pregnant women can cause abnormal brain development in their fetuses by mother-to-child transmission, which may result in miscarriage or microcephaly, however it is not yet known whether Zika virus causes microcephaly. Furthermore, a connection has been established with neurologic conditions in infected adults, including Guillain–Barre syndrome.

PLGF is a growth factor active in angiogenesis, and endothelial cell growth, stimulating their proliferation and migration. It binds to receptor vegfr-1/flt1.
PLGF-2 binds neuropilin-1 and 2 in a dependent manner.

CD70 also known as TNFSF7 is a cytokine which binds to CD27. TNFSF7 takes part in T-cell activation as well as induces the proliferation of costimulated T-cells. Moreover, TNFSF7 enhances the generation of cytolytic T-cells. Among the diseases which are associated with TNFSF7: Include acute myocarditis & Myocarditis.

Yersinia enterocolitica is a Gram-negative bacillus-shaped bacterium, which is a member of the Enterobacteriaceae family. Y.Enterocolitica is motile at temperatures between 22-29°C, however becomes non-motile at normal human body temperature. Y. Enterocolitica infection causes the yersiniosis disease, which is an animal-borne disease occurring in humans, as well as in a various groups of animals such as cattle, deer, pigs, and birds. Yersinia enterocolitica is a heterogeneous group of strains, which are conventionally classified by bio-typing into six bio-groups on the basis of phenotypic characteristics, and by serotyping into more than 57 “O” serogroups, on the basis of their O (lipopolysaccharide or LPS) surface antigen. Five of the six biogroups (1B and 2–5) are considered as pathogens. Nevertheless, only a few of these serogroups have been linked with disease in either humans or animals. Strains which belong to serogroups O:3 (biogroup 4), O:5,27 (biogroups 2 and 3), O:8 (biogroup 1B), and O:9 (biogroup 2) are most frequently isolated worldwide from human samples. Still, the main Y. enterocolitica serogroup in many European countries is serogroup O:3 followed by O:9, whereas the serogroup O:8 is mostly detected in the United States.

Fatty acid binding protein 9 (FABP9) belongs to the fatty acid-binding proteins (FABPs) which are a family of small, extremely conserved, cytoplasmic proteins to bind long-chain fatty acids and other hydrophobic ligands. FABP9 is found in midpachytene spermatocytes and round spermatids, and comprises part of the perinuclear theca. FABP9 probably links intracellular membranes and signals abnormal sperm formation during spermatogenesis.