B-hPD-1/hBTLA雙人源化小鼠~

瀏覽次數：4250　發布日期：2019-1-16　來源：本站　僅供參考，謝絕轉載，否則責任自負

hello,大家下午好啊！最近北方總是寒風陣陣，一瞅日歷，11月了！心情也隨之激動起來了有木有？咳咳，小編在此溫馨提示大家，挑仔細點！誓要成為最美買家秀知道不！

不過嘛，言歸正傳，今天的產品小鼠不過節（B-NDG已經在促銷了，再打折小編真要吃土了啊~），不多說，自產雙人源化B-hPD-1/hBTLA小鼠獻給大家~

BTLA基因功能

B細胞和T細胞衰減蛋白（B and T lymphocyte associated，BTLA）是另一種Ig超家族的檢查點負調分子，在結構上和CTLA4及PD-1類似，不僅表達于B細胞、T細胞、NK細胞，在樹突狀細胞和巨噬細胞中也有表達。BTLA與其配體HVEM（腫瘤壞死因子受體超家族成員）結合傳遞共抑制信號，在機體抗腫瘤免疫應答中發揮負性調節作用，并與腫瘤的免疫逃逸機制相關。 BTLA抑制劑可以增強TCR信號通路，并恢復T細胞功能，成為腫瘤生物治療潛在的新靶點。

Fig.1. (A) Interactions around PD1 and HVEM. PD1 belongs to the B7/CD28 (Immunoglobulin) superfamily and delivers negative signals upon binding to its ligands, PD-L1 and PD-L2. Recently, an unexpected interaction has been shown between PDL1 and CD80, whereby CD80 expressed on T cells can potentially behave as a receptor by delivering inhibitory signals when engaged by PDL1. CD80 and CD86 bind to the same two receptors, the stimulatory CD28 and the inhibitory CTL-associated-antigen-4 (CTLA-4) molecules. HVEM from the TNF/TNFR superfamily is clearly now a central immune molecule given the complexity of its interactions. HVEM has initially been discovered as the coreceptor for the glycoprotein D (gD) of the herpes simplex virus 1 (HSV-1), allowing the entry of the virus in the cell. HVEM interacts with LIGHT and lymphotoxin 3 to stimulate T cell responses. More recently, two novel ligands inhibiting T cell responses have been identified for HVEM: BTLA and CD160, a glycosphingolipid-linked protein, both belonging to the Ig superfamily, highlighting a crosstalk between the TNF-TNFR superfamily and the Ig superfamily. (B) Targeting coinhibitory molecules with monoclonal antibodies. Monoclonal antibodies (mAbs) are the primary immunotherapeutic modality used to promote immune function via antagonism or agonism of inhibitory or stimulatory molecular pathways, respectively. Cancer cells exploit the upregulation of coinhibitory molecules to inhibit T cell activation and to evade antitumor immunity. Indeed, PD1 is upregulated in TILs from many tumors and its ligands PDL1 and PDL2 are overexpressed in cancer cells. The anti-PD1 and anti-PDL1 mAbs block the interaction of PD1 with PDL1, reversing the inhibitory signaling and promoting lymphocyte activation. Similarly, high expression of BTLA was reported in tumor antigen-specific T cells from melanoma, thus BTLA would mediate inhibition of lymphocyte activation through engagement with its ligand HVEM expressed on tumors^[1].

hBTLA人源化小鼠

基本信息