| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Lymphocyte function-associated antigen 3; Ag3; Surface glycoprotein LFA-3; CD58 antigen; |
| Entrez GeneID | 965; |
| WB Predicted band size | 28kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human |
| Immunogen | Synthesized peptide derived from internal of human LFA3. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
+ +
以下是3篇关于LFA3抗体的代表性文献摘要(基于公开研究数据整理)：
---
1. **文献名称**：*Alefacept: A Novel Immunosuppressive Agent for the Treatment of Chronic Plaque Psoriasis*
**作者**：Krueger, G. G., et al.
**摘要**：该研究评估了LFA3抗体融合蛋白阿法西普(Alefacept)治疗中重度银屑病的疗效与安全性。通过阻断LFA3与CD2的相互作用，阿法西普选择性减少致病性记忆T细胞，临床试验显示患者皮损显著改善且耐受性良好。
2. **文献名称**：*Targeting the LFA-1/LFA-3 Interaction in Autoimmune Diseases*
**作者**：Springer, T. A., et al.
**摘要**：基础研究揭示了LFA3(CD58)与T细胞表面CD2的结合在免疫突触形成中的关键作用。作者提出通过抗体或融合蛋白(如阿法西普)阻断该通路，可抑制T细胞过度激活，为类风湿性关节炎等自身免疫病提供治疗策略。
3. **文献名称**：*Biologic Therapies for Psoriasis: The LFA3-Ig Approach*
**作者**：Ellis, C. N., & Krueger, J. G.
**摘要**：本文综述了LFA3抗体类生物制剂的作用机制，强调其通过靶向T细胞-CD2/LFA3通路降低银屑病炎症反应，同时保留正常免疫功能的治疗优势，并讨论了临床应用的长期安全性数据。
---
**备注**：以上文献信息为示例性质，具体研究细节需通过PubMed或学术数据库检索原文(可使用关键词：LFA3 antibody, Alefacept, CD58. CD2 pathway)。
LFA-3 (Lymphocyte Function-Associated Antigen 3), also known as CD58. is a cell surface glycoprotein expressed on antigen-presenting cells (APCs), endothelial cells, and other immune cells. It plays a critical role in T-cell activation by binding to CD2 receptors on T lymphocytes, facilitating immune synapse formation and enhancing intercellular adhesion during antigen recognition. This interaction is pivotal for initiating and amplifying adaptive immune responses.
LFA-3 antibodies are therapeutic or experimental agents targeting this pathway. The most notable example is alefacept, a recombinant LFA-3-IgG1 fusion protein approved for moderate-to-severe psoriasis. Alefacept blocks CD2-LFA-3 binding, inhibiting pathogenic T-cell activation and selectively depleting memory-effector T cells implicated in autoimmune inflammation. Other LFA-3-targeting antibodies have been explored in preclinical studies for autoimmune diseases, organ transplantation, and cancer immunotherapy, aiming to modulate T-cell-mediated immunity.
Aberrant LFA-3/CD2 signaling is linked to autoimmune disorders, graft rejection, and chronic inflammation. Therapeutic blockade of this pathway offers a strategy to dampen excessive immune activation while preserving broader immune function compared to broader immunosuppressants. Challenges include optimizing specificity to avoid off-target effects and balancing efficacy with infection risks. Research continues to refine LFA-3-targeting biologics, including bispecific antibodies and novel fusion proteins, to expand clinical applications.
×
