TRAJ18

Last update 08 May 2025

Basic Info

Synonyms

T cell receptor alpha joining 18, TRAJ18

Introduction-

100 Clinical Results associated with TRAJ18

100 Translational Medicine associated with TRAJ18

0 Patents (Medical) associated with TRAJ18

Literatures (Medical) associated with TRAJ18

20 Jun 2023·Nature communicationsQ1 · CROSS-FIELD

Tnpo3 controls splicing of the pre-mRNA encoding the canonical TCR α chain of iNKT cells.

Q1 · CROSS-FIELD

ArticleOA

Author: Sikora, Katarzyna ; Richter, Andreas S ; Boehm, Thomas ; Iwanami, Norimasa

Unconventional T cells, such as innate natural killer T cells (iNKT) cells, are an important part of vertebrate immune defences. iNKT recognise glycolipids through a T cell receptor (TCR) that is composed of a semi-invariant TCR α chain, paired with a restricted set of TCR β chains. Here, we show that splicing of the cognate Trav11-Traj18-Trac pre-mRNA encoding the characteristic Vα14Jα18 variable region of this semi-invariant TCR depends on the presence of Tnpo3. The Tnpo3 gene encodes a nuclear transporter of the β-karyopherin family whose cargo includes various splice regulators. The block of iNKT cell development in the absence of Tnpo3 can be overcome by transgenic provision of a rearranged Trav11-Traj18-Trac cDNA, indicating that Tnpo3 deficiency does not interfere with the development of iNKT cells per se. Our study thus identifies a role for Tnpo3 in regulating the splicing of the pre-mRNA encoding the cognate TCRα chain of iNKT cells.

01 Sep 2022·Journal of Investigative DermatologyQ1 · MEDICINE

Goat Milk–Derived Lipids Restrain NK T Cell–Dependent Eosinophilic Inflammation in a Murine Model of Atopic Dermatitis

Q1 · MEDICINE

Article

Author: Cait, Alissa ; Brown, Caitlin ; Gell, Katie ; Naidoo, Karmella ; Gasser, Olivier ; Carpenter, Elizabeth ; Woods, Katherine

Atopic dermatitis (AD) is a debilitating disease that disproportionately affects infants and young children and is considered the first step of the atopic march-the age-related progression of allergic disease.Consequently, there is an urgent unmet need to elucidate the root causes of AD and evaluate potential prevention mechanisms.Anecdotal evidence suggests that cow milk avoidance and substitution with other mammalian milk sources, such as goat milk (GM), has the potential to ameliorate AD symptoms.In this study, we assessed the therapeutic benefit of GM in AD in the absence of cow milk allergy and present a set of data suggesting that the noticeable therapeutic activity of GM against AD is mediated through the sensing of GM-derived lipids by NK T (NKT) cells and the effects of it on NKT cell-dependent recruitment of inflammatory eosinophils.To determine whether the consumption of GM infant formula (GMF) can decrease AD disease severity, we used a previously described MC903-driven model of AD-like disease.All strains of mice were housed under specific pathogen-free condition at the Malaghan Institute of Medical Research (Wellington, New Zealand).We compared GMF with two other GM products with contrasting lipid contents, i.e., reconstituted whole-GM powder (29.5% milk fat in dry matter) and skim GM powder (1% milk fat in dry matter).Consistent with a lipid-mediated mode of action, GMF (26% total fat, 13% milk fat in dry matter) and whole-GM powder had a similar effect on disease progression, whereas skim GM powder had no detectable activity.Because the lipid- and CD1-dependent reduction in disease severity may have been mediated by either type 1 (invariant) or type 2 NKT cells, we compared Cd1-/- mice, which are deficient in both types of NKT cells, with mice lacking the invariant NKT (iNKT) cell receptor a -chain gene segment TRAJ18 ( Ja 18-/-), which express CD1 but lack iNKT cells.Together, these results suggest that consumption of full-fat GM products can have a beneficial effect on AD disease severity, possibly by restraining iNKT cell-dependent eosinophilia.However, because the MC903 AD- like model is conducted in the absence of allergen, the therapeutic effect of dietary NKT-cell modulation in disease settings comprising allergen-specific T helper 2 cells and/or addnl. alarmins (e.g., IL-33) remains to be determinedFinally, further research is warranted to appropriately compare GM with cow and human milk and determine the interspecies variations in milk-derived NKT cell modulators.

01 Jun 2019·ImmunoHorizons

Deficiency of Mucosal-Associated Invariant T Cells in TCRJα18 Germline Knockout Mice

Article

Author: Pan, Yun ; Chen, Yongping ; Xie, Jinhai ; Gao, Jimin ; Wang, Peng ; Tao, Huishan ; Zhong, Xiao-Ping

AbstractMucosal-associated invariant T (MAIT) cells and invariant NK T (iNKT) cells account for the major lymphocyte populations that express invariant TCRα-chains. MAIT cells mostly express the TCRVα19-Jα33 TCR in mice and the TCRVα7.2-Jα33 TCR in humans, whereas iNKT cells express the TCRVα14-Jα18 TCR in mice and the TCRVα24-Jα18 TCR in humans. Both MAIT and iNKT cells have the capacity to quickly produce a variety of cytokines in response to agonist stimuli and to regulate both innate and adaptive immunity. The germline TCRJα18 knockout (Traj18−/−) mice have been used extensively for studying iNKT cells. Although it has been reported that the TCRα repertoire was narrowed and the level of Trav19-ja33 transcript was decreased in this strain of mice, direct assessment of MAIT cells in these mice has not been reported. We demonstrate in this study that this strain of mice is also defective of MAIT T cells, cautioning data interpretation when using this strain of mice.

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TRAJ18

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