anti-Interferon, gamma-Inducible Protein 30 (IFI30) Antibodies

Zebrafish Interferon, gamma-Inducible Protein 30 (IFI30) interaction partners

1. GILT expression is up-regulated in spleen and kidney after immunization with LPS although it also is constitutively expressed in heart, liver, muscle and intestine, suggesting that GILT may be involved in the immune response to bacterial challenge.

Mouse (Murine) Interferon, gamma-Inducible Protein 30 (IFI30) interaction partners

1. GILT has a role in maintaining cysteine cathepsin proteolytic efficiency in phagosomes

2. These results show that wild-type mouse fibroblasts are relatively resistant and GILT(-/-)mouse fibroblasts are susceptible to Dengue virus 2 entry and replication.

3. Data indicate that in the absence of Gamma-interferon-inducible lysosomal thiol reductase (GIL, CD4-positive T cell responses to major house dust mite allergen Der p 1 are significantly reduced.

4. GILT has a critical role in regulating CD4(+) T-cell tolerance to an endogenous skin-restricted antigen relevant to controlling autoimmunity and generating effective immunotherapy for melanoma.

5. gene knock-outs increase oxidative stress and autophagy, which is regulated by altering glutathione synthesis and oxidation

6. We showed that STAT1 interacts with the GILT promoter, even in the absence of IFN-gamma, and that STAT1 represses GILT expression.

7. GILT has limited yet unexpected effect on self-peptide species presented by major histocompatibility complex class II antigens.

8. study shows GILT facilitates MHC class I-restricted recognition of exogenous antigens containing disulfide bonds by CD8+ T cells or cross-presentation;initiation of gB-specific CD8+ T cell response during HSV-1 infection or cross-priming is GILT-dependent

9. the thiol reductase activity of GILT is its essential function in MHC class II-restricted Ag processing

10. GILT appears to have a fundamental role in cellular proliferation mediated through its influence on SOD2 protein activity and expression.

11. findings show that endogenously produced peptide-IgG is processed by transduced splenic B cells in the lysosomes/endosomes in a GILT-dependent manner, and this endocytic processing pathway is essential for generating tolerogenic B cells

12. Replication of Listeria monocytogenes in GILT-negative macrophages, or macrophages expressing an enzymatically inactive GILT mutant, is impaired because of delayed escape from the phagosome

13. Expression of GILT in T-lymphocytes increases as a function of maturity, thereby reducing sensitivity of T-cells and consequences of autoimmune responses; a role of GILT in the immune system may be in reducing the impact of T-cell autoreactivity.

14. GILT facilitated the processing and presentation to antigen-specific T cells of protein antigens containing disulfide bonds.

Human Interferon, gamma-Inducible Protein 30 (IFI30) interaction partners

1. GILT was highly expressed as observed in the public database on human gliomas and two human glioma cell lines, U373MG and U87MG cells. The downregulation of GILT by lentiviral-mediated silencing inhibits the cell growth, colony formation, and migration but promotes apoptosis and results in cell cycle arrest at the G0/G1 phase in the U373MG cells.

2. Results shows that GILT expression is required for downregulation of PAX-3 proteins in late stage human melanoma cells. GILT co-localizes with PAX-3 proteins regulating its expression through the autophagy and lysosomal degradation pathway in human melanoma cells.

3. GILT functions as a host restriction factor against the retroviruses.

4. GILT expression is anticipated to result in improved presentation of melanoma antigens and more effective antimelanoma T-cell responses.

5. The lysosomal thiol reductase GILT expressed by antigen-presenting cells has diverse cellular and organismal functions. (Review)

6. this review discusses recent studies that have advanced our understanding of the role of GILT in antigen processing and revealed surprising new functions for the enzyme.[review]

7. Single nucleotide polymorphism of the interferon-gamma-inducible protein 30 gene is associated with hyperglycemia in severely obese individuals.

8. GILT is required for efficient histocompatiblity class II-restricted processing of melanoma antigen tyrosinase-related protein 1 epitope in vitro and accelerates the onset of vitiligo in TRP1-specific T-cell receptor transgenic mice.

9. Absence of gamma-interferon-inducible lysosomal thiol reductase in melanomas disrupts T cell recognition of select immunodominant epitopes.

10. Role of the C-terminal propeptide in the activity and maturation of gamma -interferon-inducible lysosomal thiol reductase (GILT).

11. GILT-expressing melanoma cells could prove to be very promising for direct antigen presentation and CD4+ T cell recognition

12. studied gene expression profile of brain lesions of a patient with Neuromyelitis optica by using DNA microarray; found marked up-regulation of interferon gamma-inducible protein 30 (IFI30), CD163, and secreted phosphoprotein 1 (SPP1, osteopontin)

Pig (Porcine) Interferon, gamma-Inducible Protein 30 (IFI30) interaction partners

1. The cloning and characterization of porcine gamma-interferon-inducible lysosomal thiol reductase (GILT) are reported.