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Lymphotoxin-alpha (LT-alpha or LTA) belongs to the TNF ligand superfamily, which bind the same TNF receptor and mediate similar pleiotropic effect. LTA is a proinflammatory cytokine with important biological activity and immunomodulatory function and is known to influence a variety of cellular response. Furthermore, LTA mediates a large variety of inflammatory, immunostimulatory, and antiviral responses, is involved in the formation of secondary lymphoid organs during development and has a role in apoptosis. LTA is highly inducible, secreted, and forms heterotrimers with lymphotoxin-beta which anchors lymphotoxin-alpha to the cell surface. LTA, which is located within the MHC III region of chromosome 6, shows close relation to the HLA class I (HLA-B) and class II (HLA-DR) genes. Polymorphism in the LTA gene appears to contribute to infectious disease susceptibility and infection. Genetic variations in the LTA gene are linked to susceptibility to leprosy type 4 and psoriatic arthritis.

Chitinase 3-Like 2 (CHI3L2) is similar to bacterial chitinases but lacks chitinase activity. CHI3L2 protein is secreted and is involved in cartilage biogenesis. CHI3L2 is a lectin, which binds chitooligosaccharides and other glycans with high affinity, but not heparin.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNAvirus in the family Flaviviridae. HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, the HCV has an exceptionally high mutation rate, a factor that may help it elude the host's immune response. Hepatitis C virus is classified into six genotypes(1-6) with several subtypes within each genotype. The preponderance and distribution of HCV genotypes varies globally. Genotype is clinically important in determining potential response to interferon-based therapy and the required duration of such therapy. Genotypes 1 and 4 are less responsive to interferon-based treatment than are the other genotypes (2, 3, 5 and 6).

CD21 is expressed strongly on mature B cells, follicular dentritic cells and weakly on immature thymocytes and T lymphocytes. In B-cell ontogeny, CD21 appears after the pre-B-stage, is maintained during peripheral B-cell development and is lost upon terminal differentiation into plasma cells. CD21 expression is also gradually lost after stimulation of B cells in vitro. CD21 functions as receptor for C3d, C3dg and iC3b Complement components, for EBV and for IFNalpha. CD21 binds to CD23 and associates with CD19, CD81 and Leu13 to form a large signal-transduction complex involved in B cell activation.

Chemokine (C-X-C motif) ligand 5 (CXCL5) is a small cytokine belonging to the CXC chemokine family that is also known as epithelial-derived neutrophil-activating peptide 78 (ENA-78). It is produced following stimulation of cells with the inflammatory cytokines interleukin-1 or tumor necrosis factor-alpha. Expression of CXCL5 has also been observed in eosinophils, and can be inhibited with the type II IFN. This chemokine stimulates the chemotaxis of neutrophils possesses angiogenic properties. It elicits these effects by interacting with the cell surface chemokine receptor CXCR2. The gene for CXCL5 is encoded on four exons and is located on human chromosome 4 amongst several other CXC chemokine genes. CXCL5 has been implicated in connective tissue remodelling.

H3N2 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteinson the surface of its coat, hemagglutinin(H) and neuraminidase(N). H3N2 exchanges genes for internal proteins with other influenza subtypes. H3N2 has tended to dominate in prevalence over H1N1, H1N2, and influenza B. H3N2 strain descended from H2N2by antigenic shift, in which genes from multiple subtypes re-assorted to form a new virus. Both the H2N2and H3N2 strains contained genesfrom avian influenzaviruses.

The Defensin family are highly similar in their protein sequence and are microbicidal & cytotoxic peptides made by neutrophils. Beta Defensin-1 is an antimicrobial peptide having the resistance of epithelial surfaces to microbial colonization. Beta Defensin-1 has close proximity to Defensin Alpha-1 and has been implicated in the pathogenesis of cystic fibrosis.
Skin of patients having atopic dermatitis patients and mycosis fungoides (non-lesional and lesional) show lower human Beta Defensin-1 mRNA expression and higher human Beta Defensin-2 and human Beta Defensin-3 mRNA expression.
Beta Defensin is highly expressed by epithelial cells.
Beta-defensin 1 may play a role in the pathogenesis of severe sepsis.

The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contributes to the clonal expansion, survival, and development of T cells. It can also induce proliferation in peripheral monocytes, enhance T cell apoptosis induced by TCR/CD3 triggered activation, and regulate CD28 co-stimulation to promote Th1 cell responses. The expression of this receptor is induced by lymphocyte activation. TRAF adaptor proteins have been shown to bind to this receptor and transduce the signals leading to activation of NF-kappaB.

Shiga-like toxin (verotoxin) is a toxin produced by some strains of Escherichia coli. Shiga-like toxin is named for its similarity to the AB5-type Shiga toxin produced by the bacteria Shigella dysenteriae. There are two known types-SLT1 and SLT2. The Shiga-like toxin is linked with hemolytic-uremic syndrome. Shiga-like toxin requires highly specific receptors on the cells'' surface in order to attach and enter the cell. Species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, dropping them in their feces, from where they may be distributed to humans. Shiga Like Toxin-1 Subunit B has nontoxic action, it is the functional region which binds to the receptor. The Shiga Like Toxin-1 Subunit B can be useful in vaccine study, antibody test and other functional research.

Caused by one of four closely related virusserotypesof the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. In cell culture experiments and mice Morpholinoantisense oligos have shown specific activity against Dengue virus.

Entry of HSV into the host cell involves interactions of several viral glycoproteins with cell surface receptors. The virus particle is covered by an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane and create an opening, or pore, through which the virus enters the host cell. The sequential stages of HSV entry are analagous to those of other viruses. At first, complementary receptors on the virus and cell surface bring the two membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell.

Receptors across the cell membrane interact with some viral glycoproteins therefor enabling HSV to enter the host cell. The HSV enter through pores created by the binding of particular receptors across the cell membrane with the virus's coating envelope, following by a fusion of the HSV and the host cell. HSV enters the host cell through the same mechanism and stages as other viruses do. Initially, matching receptors across the virus's envelope and host cell's membrane interacts and bring the two together. During the transitional stage, begins fusion between the host cell and virus (hemifusion state). The closing stage happens when a steady pore was made; through these pores the virus's particles enter the cell.

Regulated upon Activation, Normal T-cell Expressed, and Secreted or RANTES is an 8 kDa protein classified as a chemotactic cytokine or chemokine. It has recently been renamed CCL5. RANTES is chemotactic for T cells, eosinophils and basophils and plays an active role in recruiting leukocytes into inflammatory sites. With the help of particular cytokines (i.e. IL-2 and IFN-?) that are released by T cells, RANTES also induces the proliferation and activation of certain natural killer (NK) cells to form CHAK (CC-Chemokine-activated killer) cells. It is also a HIV-suppressive factor released from CD8+ T cells. This chemokine has been localized to chromosome 17 in humans.

HBsAg is the surface antigen of the Hepatitis-B-Virus (HBV). The capsid of a virus has different surface proteins from the rest of the virus. The antigen is a protein that binds specifically on one of these surface proteins. It is commonly referred to as the Australian Antigen.

GroEL, HSP60 is a chaperonin located in the mitochondria which is responsible for the transportation & refolding of proteins from the cytoplasm directly into the mitochondrial matrix. GroEL is regulated by the HSP10 cochaperonin, which is a single heptameric protein ring having a molecular mass of 10 kDa which form a unique complex with HSP60. HSP10, GroES coordinates the ATPase activity of the HSP60 subunits in order to allow the release of bound polypeptide in a manner that is productive for its correct folding.

CCL25 (Teck) is a novel CC chemokine, which is distantly related (about 20% amino acid sequence identity) to other CC chemokines. The mouse CCL25 cDNA has also been cloned and shown to encode a 144 a.a. protein, which exhibits 49% a.a. sequence identity to the human CCL25. Human and mouse CCL25 expression was shown to be greatly restricted to the thymus and small intestine. While dendritic cells are identified as the source of CCL25 production in the thymus, dendritic cells derived from bone marrow do not express CCL25. CCL25 signals through the CCR9 receptor. Teck is possibly involved in T-cell development.
Recombinant human and mouse Teck were shown to be chemotactic for activated macrophages, dendritic cells and thymocytes. The recombinant protein demonstrates chemotactic activity on thymocytes, macrophages, THP-1 cells, and dendritic cells but is inactive on peripheral blood lymphocytes and neutrophils.

Human immunodeficiency virus (HIV) is a retrovirusthat can lead to a condition in which the immune systembegins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the humanimmune systemsuch as helper T cells(specifically CD4+ T cells), macrophagesand dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosisin infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytesthat recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections. HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genomeis converted to double-stranded DNAby a virally encoded reverse transcriptasethat is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latentand the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

Human immunodeficiency virus (HIV) is a retrovirusthat can lead to a condition in which the immune systembegins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the humanimmune systemsuch as helper T cells(specifically CD4+ T cells), macrophagesand dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosisin infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytesthat recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections. HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genomeis converted to double-stranded DNAby a virally encoded reverse transcriptasethat is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latentand the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

CD200R1, also known as cell surface glycoprotein CD200 receptor 1, is an isoform of CD200 receptors which is expressed on cells of the myeloid lineage. CD200R1 inhibitory signaling pathway has been involved in taking a prominent role in limiting inflammation in a broad range of inflammatory diseases. CD200R1 signaling inhibits the expression of proinflammatory molecules including tumor necrosis factor, interferons, in addition to inducible nitric oxide synthase in response to selected stimuli.

LSM5 also known as LSM5 Homolog, U6 Small Nuclear RNA Associated belongs to the Sm protein family. This family is identified in a variety of organisms based on sequence homology. Sm-like proteins contain the Sm sequence motif, which consists of 2 regions separated by a linker of variable length which folds as a loop. In addition, the Sm-like proteins are thought to create a stable heteromer present in tri-snRNP particles, which are important for pre-mRNA splicing. Among the diseases associated with LSM5 are spinal muscular atrophy, and muscular atrophy.

Interleukin-3 is a pleiotropic cytokine produced primarily by activated T cells.
IL-3 is thought to function via specific cell surface receptors to stimulate the proliferation, differentiation and survival of haematopoietic cell lines. IL-3 has also been shown to affect the functional activity of a variety of other cell types including mast cells, eosinophils, megakaryocytes and basophils.

Methicillin-resistant Staphylococcus aureus, MRSA bacterium also be referred to as multiply-resistant Staphylococcus aureus or oxacillin-resistant Staphylococcus aureus, ORSA, evolved the ability to survive treatment with beta-lactam antibiotics, including penicillin, methicillin, and cephalosporins. Common strains of MRSA are EMRSA15 and EMRSA16.EMRSA16 is best described epidemiologically & found to be identical to the ST36:USA200 strain. Under the new international typing system, ST36:USA200 strain is now called MRSA252. It is not entirely certain why this strain has become so successful, whereas previous strains have failed to persist. One explanation is the characteristic pattern of antibiotic susceptibility. Both the EMRSA15 and EMRSA16 strains are resistant to erythromycinand ciprofloxacin. It is known that Staphylococcus aureus can survive intracellularly, and these are precisely the antibiotics that best penetrate intracellularly; it may be that these strains of S. aureus are therefore able to exploit an intracellular niche. Most cases of CA-MRSA are caused by a CC8 strain designated ST8:USA300, which carries mec type IV, Panton-Valentine leukocidin, PSM-alpha and enterotoxins Q and K,and ST8:USA400. Other community-associated strains of MRSA are ST8:USA500 and ST59:USA1000.

IL36RA belongs to the IL-1 family of proteins. IL36RA is produced as a 156 aa protein which holds no signal sequence, no prosegment and no potential N-linked glycosylation site but, IL36RA is secreted as a 17 kDa monomer. Cells known to express IL36Ra/IL1F5 include monocytes, B cells, keratinocytes, dendritic cells/Langerhans cells and gastric fundus Parietal and Chief cells.