Tslp Antibodies

Thymic stromal lymphopoietin (Tslp)

Cytokine that induces the release of T-cell-attracting chemokines from monocytes and, in particular, enhances the maturation of CD11c(+) dendritic cells. Can cause allergic inflammation by directly activating mast cells (By similarity).

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Gene Information

Mouse
Gene Name:	Tslp
Uniprot:	Q9JIE6
Entrez:	53603

Family

Belongs to:
No superfamily

Alternative Names

thymic stromal lymphopoietin; TSLP

Molecular Weight

Mass (kDA):
16.152 kDA

Genomic Context

Mouse
Location:	18 B1|18 18.12 cM
Sequence:	18;

Diseases

• Inflammation
• Asthma
• Dermatitis, Atopic
• Dermatitis
• Allergy
• Rhinorrhea
• Allergic Asthma
• Allergic Rhinitis (disorder)
• Lung Diseases
• Dermatologic Disorders
• Virus Diseases
• Neoplasms
• Pneumonia

• Lung Diseases, Obstructive
• Malignant Neoplasms
• Chronic Obstructive Airway Disease
• Eosinophilia
• Autoimmunity
• Hyperplasia
• Colitis

Pathways

• Pathogenesis
• Immune Response
• Sensitization
• Cytokine Production
• Secretion
• Cell Development
• Cell Activation
• Cell Proliferation
• Cell Differentiation
• T Cell Homeostasis
• Cytokine Secretion
• Inflammatory Response
• Hypersensitivity

• Adaptive Immune Response
• Cell Maturation
• Innate Immune Response
• Glycosylation
• Cell Migration
• T Cell Activation
• Skin Development

PTMs

• Phosphorylation
• Glycosylation

• Cleavage
• Acetylation

• Deglycosylation

Research Areas

• Innate Immunity

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Tslp

Boster Bio - Best Uses Of The TSLP Marker

TSLP is a cytokine corresponding to IL-7. It affects both the cellular and humoral immune systems , and has many potential uses. TSLP has been demonstrated to promote chemotaxis, delay the process of apoptosis and improve humoral immunity. However, the precise role isn't fully understood. Let's review some of the best uses for this marker.

TSLP is a cytokine related to the IL-7.

TSLP, an IL-7-related cytokine, is found in epithelial cell lines of patients suffering from chronic rhinosinusitis and asthma. It is also associated with increased susceptibility to Atopic skin dermatitis. This cytokine that is produced by DCs and is essential to the development and maintenance of Th2 immune responses. TSLP has two isoforms: short and long and has various proinflammatory properties.

TSLP is a novel cytokine , which was initially isolated from murine thymic stromal cells. The TSLP gene product helps in the growth, differentiation, and expansion of T and B cells. TSLP contains a heterodimeric receptor that is comprised of an IL-7R–a as well as an g-receptor-like common chain.

The TSLP gene is found in a range of tissues, including lung cancer cells. It is present in lung cancer tissues at a higher degree than its normal counterpart. Additionally, TSLP-DCs have STAT-1,-3, and 5, phosphorylated which facilitates the recruitment of Treg cells and their differentiation. TSLP expression was also linked to tumor-derived TSLP in the lung.

A variety of types of tumors have suggested that TSLP might play an anti-tumor effect. TSLP expression was linked to anti-tumor effects in mice. Its anti-tumor effects are also observed in cancer cell lines. Further research is required to determine the anti-tumor function of TSLP in tumors. There is no commercial relationship or financial interests to disclose. The Italian Ministry of Health has funded the research described in this article.

Although the function of hTSLP remains unclear, it has been shown that it can stimulate the mTOR pathway, as well as B-cell precursors. Utilizing mice with CRLF2-deficient genes as an example of hTSLP, it provides the possibility of a cross-species xenograft. Therefore, TSLP is an exciting new drug for cancer treatment. With continued research it will be possible to discover how TSLP can be used in patients with lymphoma and B-cell leukemia.

It induces chemotaxis

The Boster Bio TSLP marker triggers Eosinophil degranulation in vitro. These results were compared to an uninhibited control affected by TSLP. Both the positive control cells as well as the unstimulated control cells produced Eosinophils at the same rate. These results support the concept that TSLP is a potent marker in chemotaxis.

The human thymic stromal cytokine (TSLP) is a cytokine predominantly produced by epithelial cell. It has been identified as the cause of allergic rhinitis (Asthma) and bronchitis. Allergy airway inflammation is caused by TSLP expression in mouse keratinocytes. Therefore, TSLP may be a major factor in the transition from AD to AR.

In addition the Boster Bio TSLP marker triggered a Th2 response in mouse mDCsand thereby increasing the frequency of IL-4, IL-5, and IL-13-producing cells. The TSLP-induced Th2 responses are dependent upon OX40L expression on the mDCs. Curdlan decreased mDCs' Th2 response by increasing IL-10 expression.

In addition to chemotaxis, TSLP can activate eosinophil degranulation. Compared to the effects of IL-5 or GM-CSF, TSLP significantly increases EDN release. In addition, TSLP stimulation is similar to the effects of the IL-5 or IL-10 in 10 ng/ml. This effect is dose-dependent.

The mast cells produce the TSLP protein, which is a pro-inflammatory protein that is involved in allergic inflammation. Furthermore the TSLP gene, which is expressed in mast cells as well as other types of cells is known to influence the chemotaxis and chemotaxis of Eosinophils. In in vitro, TSLP mDCs are able to keep CRTH2 expression after activation. These results are in line with other studies.

It is apoptosis-related.

The TSLP marker inhibits apoptosis in two ways. First, it binds to the Fas pathway protein kinase, which is involved in the death of cells caused by DNA damage. The second is that it interacts with the protein BclXL, which regulates apoptosis. It also interacts with CLARP, which regulates the apoptosis process.

In a recent study, researchers discovered that the TSLP marker delayed the apoptosis process in colorectal cancer cells. This protein, also known by PUMA which slows the process of apoptosis, occurs when it responds to the signaling of p53. These cells also express Fas, a death receptor cell that is essential for apoptosis.

The BH-3 only protein (Bik), an ally of the gene family as caspases, is also a brand new member of the TSLP families. Its structure and activity are identical to the caspase-3, but differ in the cell-specific domain. It is also activated by various cell death triggers, such as cell cycle stop and Apoptosis. The activation of Bax and Bak disrupts mitochondrial function and releases pro-apoptotic substances into the cytoplasm. Apoptosis also occurs due to activation of downstream caspases.

While apoptosis is necessary for many multicellular organisms, it is critically important for the development and function of T lymphocytes. Anti-CD3 stimulation results in a reduction of 10% in apoptosis rates in genetically deficient mice than in WT mice. These findings suggest that the extrinsic pathway could be involved. These findings require further investigation.

It affects the humoral immunity

Researchers examined the immune system in order to determine the way in which the TSLP marker affects humoral immunity. They exposed mice to a TSLP-containing vaccine, 100 mg of neutralizing antibody to TGF-b, or PBS by itself. After 48 hours, dendritic cells were isolated. They discovered that TSLP affected DCs' function, differentiation, and response to antigen. These findings suggest that TSLP may influence humoral immunity.

Researchers have also discovered that the TSLP marker may affect the immune response in mice as well as humans. The interaction between TSLP and TSLPR is crucial for triggering Ag-specific IgA responses. TSLP also enhances TFH differentiation, as well as the humoral response. More research is required to understand the precise role that TSLP is playing in the process of enhancing humoral immunity. It is vital to research TSLP signaling to create better mucosal vaccines.

In a mouse model, TSLP expression was associated with an increase in serum TSLP. This marker hinders the production and maintenance of B cells. Additionally, increased TSLP levels resulted in a decrease in B cells as well as a significant rise in non-hematopoietic lineages like basophils, mast cells, and dendritic cell lines. In mice the elevated levels of TSLP also led to the development of atopic dermatitis and hemolytic anemia autoimmune.

TSLP is also involved in the development of type 2 inflammation. It is also involved in other diseases like autoimmunity, infections and cancer. Detailed studies are needed to establish the exact function of TSLP in the various kinds of inflammation that occur in humans. These findings will assist researchers understand how TSLP affects the humoral immune system and the various pathways through which it may influence the progression of diseases.

It is over-expressed by patients with Netherton syndrome.

TSLP is a gene that has been implicated in various allergic disorders, including Netherton syndrome. Netherton syndrome is characterized by an atopic dermatitis-like lesions and other allergic manifestations. Netherton syndrome patients have TSLP over-expressed. A mutation in the Kazal-type 5-gen causes TSLP overexpression.

A genetic disorder that is characterized by a triple triad of clinical symptoms (eczema and congenital ichthyosiform epidermal erythroderma, and immune dysregulation), Netherton syndrome is caused by loss-of function mutations in the SPINK5 gene which encodes a proteins inhibitor called LEKTI that blocks lymphoepithelial Kazal-type-related inhibitor. Netherton syndrome patients suffer from severe skin problems that include ichthyosis linea circumflexa and superficial scaling. While the pathogenesis of Netherton syndrome remains unknown it is essential to identify the condition early for the proper treatment and management of this disorder. A multidisciplinary approach is needed to determine the root causes of the syndrome and create the most effective treatment plan.

Netherton syndrome sufferers have TSLP that is over-expressed in eosinophils and mast cells. These cells produce Th2-type cytokines. In addition to inducing the TSLPR in these cells, TSLP has been associated with inflammation processes such as asthma, allergies and Atopic skin rashes.

Numerous studies have proven that TSLP overexpression is associated with various autoimmune diseases. Particularly, the inducible and permanent overexpression of TSLP has been linked to cryoglobulinuria, kidney inflammation and increased production of systemic polyclonal IgM and IgG. TSLP can also be involved in eosinophilic esophagitis.