TL1A, a TNF superfamily member, plays a key role in autoimmune diseases. Sino Biological offers recombinant TL1A proteins with diverse tags and species to support related research.
TL1A is primarily expressed by endothelial cells, macrophages, dendritic cells, and lymphocytes. It is inducible by inflammatory cytokines such as TNF and IL-1β, and its expression can be stimulated through interactions with immune complexes and toll-like receptor signaling[1]. TL1A functions as a potent modulator of immune cell activity, significantly influencing T-cell proliferation and cytokine production. It acts on a variety of immune cells, enhancing their response capabilities and playing a pivotal role in the inflammatory cascade.
The role of TL1A extends beyond normal immune modulation, as it is critically involved in pathological conditions where its elevated expression is associated with disease severity and progression. In diseases like inflammatory bowel disease (IBD) and psoriasis, TL1A contributes to the inflammatory milieu by promoting Th1 and Th17 responses, which are key to the disease mechanisms[1, 2].
TL1A connects innate immune responses to adaptive immune responses and is critically involved in the induction of autoimmune and inflammatory diseases[3].
The interaction between TL1A and its receptor, death receptor 3 (DR3), is central to its function. This binding initiates a cascade of intracellular signaling that promotes inflammation rather than apoptosis. DR3 contains a death domain, but the primary outcome of its engagement is the activation of NF-kB and MAPK pathways, leading to the production of pro-inflammatory cytokines such as IFN-γ and IL-17. TL1A also synergizes with other cytokines like IL-12 and IL-18 to enhance IFN-γ production, which biases the immune response towards a Th1 phenotype. This interaction is crucial for its role in exacerbating inflammatory responses in autoimmune diseases such as rheumatoid arthritis (RA) and IBD, where a Th1/Th17-skewed immune response is a hallmark[3].
TL1A’s significant role across various immune-mediated diseases has been well documented, highlighting its involvement in autoimmune and inflammatory disorders like rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and psoriasis[4]. Understanding its application in these conditions helps elucidate potential therapeutic approaches that target TL1A-mediated pathways.
In RA, TL1A is upregulated and contributes to the pathogenic process by enhancing the proliferation of memory T cells and the production of inflammatory cytokines. Elevated levels of TL1A have been correlated with increased disease activity and severity, particularly in patients who are rheumatoid factor (RF) positive . Experimental models demonstrate that manipulating TL1A levels can affect disease outcomes, suggesting that TL1A could be a viable target for therapeutic intervention. Inhibition of TL1A has shown potential in reducing inflammation and joint destruction in RA models[5].
TL1A’s role in IBD highlights its influence on gut immunity. It has been shown to exacerbate inflammatory responses in the gut by promoting the differentiation and activity of Th1 and Th17 cells, which are key contributors to the chronic inflammation observed in IBD. Elevated TL1A expression in the intestinal mucosa correlates with disease severity and response to therapy, underscoring its potential as a biomarker and therapeutic target in managing IBD[6].
In psoriasis, TL1A contributes to skin inflammation by driving Th17 cell differentiation and cytokine production, particularly IL-17, which is crucial in the pathophysiology of psoriasis. Increased expression of TL1A in psoriatic lesions has been linked to disease activity, suggesting that targeting TL1A could reduce the inflammatory burden and improve clinical outcomes in psoriasis patients[1].
| Cat# | Species | Purity | Tag |
| 17049-H56H2-B | Human | ≥ 95% SDS-PAGE, ≥ 90% SEC-MALS | His & AVI Tag |
| 17049-H01H | Human | > 95% SDS-PAGE | hFc Tag |
| 17049-H07H | Human | > 95% SDS-PAGE | His Tag |
| 17049-H04H | Human | > 90% SDS-PAGE | mFc Tag |
| 17049-H15H | Human | > 90% SDS-PAGE | rFc Tag |
| 5A7685-M07H1 | Mouse | ≥ 95% SDS-PAGE, ≥ 90% SEC-MALS | His Tag |
| 80150-R07H | Rat | ≥ 95% SDS-PAGE, ≥ 90% SEC-HPLC, ≥ 90% SEC-MALS | His Tag |
| 80150-R01H | Rat | > 90% SDS-PAGE | hFc Tag |
1. Migone TS, Zhang J, Luo X, et al. TL1A is a TNF-like ligand for DR3 and TR6/DcR3 and functions as a T cell costimulator. Immunity. 2002;16(3):479-492. doi: 10.1016/s1074-7613(02)00283-2
2. Kokkotis G, Bamias G. TL1A as a therapeutic target in inflammatory bowel disease. Expert Rev Clin Immunol. 2022;18(6):551-555. doi:10.1080/1744666X.2022.2074401
3. Aiba Y, Nakamura M. The role of TL1A and DR3 in autoimmune and inflammatory diseases. Mediators Inflamm. 2013;2013:258164. doi:10.1155/2013/258164
4. Xu WD, Li R, Huang AF. Role of TL1A in Inflammatory Autoimmune Diseases: A Comprehensive Review. Front Immunol. 2022;13:891328. Published 2022 Jul 14. doi:10.3389/fimmu.2022.891328
5. KBayry J. Immunology: TL1A in the inflammatory network in autoimmune diseases. Nat Rev Rheumatol. 2010;6(2):67-68. doi:10.1038/nrrheum.2009.263
6. Solitano V, Jairath V, Ungaro F, Peyrin-Biroulet L, Danese S. TL1A inhibition for inflammatory bowel disease treatment: From inflammation to fibrosis. Med. 2024;5(5):386-400. doi:10.1016/j.medj.2024.03.010
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