Regulation and biological impact of IL-17 production by gamma delta T cells

γ δ T 细胞产生 IL-17 的调节和生物学影响

基本信息

批准号：
7897748
负责人：
Yueh-Hsiu Chien
金额：
$ 40.96万
依托单位：
STANFORD UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2009
资助国家：
美国
起止时间：
2009-07-22 至 2011-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7897748
关键词：
Acute Affect Antibody Formation Antigens Area Asthma Autoimmune Diseases Autoimmunity B-Cell Development B-Lymphocytes Biological Bone Marrow C57BL/6 Mouse CD4 Positive T Lymphocytes Cell physiology Cells Competence Cytokine Receptors Dendritic Cells Development Encephalomyelitis Experimental Autoimmune Encephalomyelitis Freund&apos s Adjuvant Goals Helper-Inducer T-Lymphocyte Histocompatibility Antigens Class I IL17 gene IgE Immune Immune response Immunization Infection Inflammation Inflammatory Inflammatory Response Injection of therapeutic agent Interleukin-17 Interleukin-4 Ligands Lymphocyte Function Mediating Molecular Mus Myelin Proteins Myelogenous Neutrophil Infiltration Ovalbumin Pathology Pattern Peptides Play Population Post-Transcriptional Regulation Process Production Regulation Reporting Resolution Role Serum Severities Signal Transduction Site Source Specificity Staging Structure of germinal center of lymph node System T cell response T-Lymphocyte Tea Thymus Gland Tissues Transcriptional Regulation Vertebrates Wild Type Mouse abstracting antigen processing cytokine experience fighting lymph nodes mRNA Stability macrophage monocyte mouse model neutrophil oligodendrocyte-myelin glycoprotein ovalbumin-alum programs research study response secondary infection subcutaneous

项目摘要

Program Director/Principallnvestigator (Last, First, Middle): Chien, Yueh-Hsiu Program Director/Principal Investigator (Last, First, Middle): Chien, Yueh-Hsiu 1 R01 A1080829-O1AI I ROl AI080829-01 A 1 ABSTRACT Inflammation is a rapid response to tissue damage and/or infection. While it is largely an innate Inflammation a rapid response to tissue damage infection. While is largely an innate response during its initial stages, in vertebrates, it has evolved to require a T ceU cytokine, IL-17, in it has evolved to require a T cell cytokine, to promote the expansion of neutrophils and monocytes in the bone marrow and their release and recruitment to sites of inflammation. This process strengthens the inflammatory cascade to to sites inflammation. This process strengthens the inflammatory cascade to signal, eradicate the injurious signal, starts the resolution program and launches the adaptive immune (U) =w' response. Our previous experiments suggested that El EIIT cellsare uniquely suited to mount an experiments suggested that 0 I;J T cells are uniquely suited to mount an response. IL-17 response at the onset of acute inflammation and we found that E1II1J cells are the major ILonset of acute inflammation and we found that DCTr cells are the IL IL-17 17+ population at the onset of CFA immunization.. While the development of IL-i 7f Li LIT cells has immunization the development of IL-17:tDI;J T cells 17+ population regulated in DI;:JT been well documented, little is known about how IL-17 is regulated in[ILIT cells. Furthermore, documented, deficier)to LiT responses have been noted in although deficientLi l;JT responses have been noted in mice lackingD I;JT cells, the possibility lacking LI1T cells, the possibility thqtthese cells act early in an inflammatory response to affect the priming process has not been in thatthese priming been explored. We will investigate these areas, which are of fundamental importance in understanding explored. will areas, which fundamental in understanding host immune defense. defense. -,Q" .2) =-0 0 pay .L., E'6 --6 ,tea 0-0 ono

项目主任/主要研究者（姓、名、中）：简月修项目主任/首席研究员（姓、名、中）：简月修 1 R01 A1080829-O1AI I ROl AI080829-01 A 1 摘要炎症是对组织损伤和/或感染的快速反应。虽然它很大程度上是一种先天性炎症，是对组织损伤感染的快速反应。虽然在其初始阶段很大程度上是一种先天反应，但在脊椎动物中，它已经进化到需要 T 细胞细胞因子 IL-17，因为它已经进化到需要 T 细胞细胞因子来促进骨中中性粒细胞和单核细胞的扩张骨髓及其释放和募集到炎症部位。这个过程增强了炎症部位的炎症级联反应。这个过程加强了炎症级联信号，消除有害信号，启动解决程序并启动适应性免疫 (U) =w' 回复。我们之前的实验表明，El EIIT 细胞特别适合产生反应。实验表明，0 I;J T 细胞特别适合产生反应。急性炎症发作时的 IL-17 反应，我们发现 E1II1J 细胞是急性炎症的主要 ILonset，我们发现 DCTr 细胞是 CFA 免疫开始时的 IL IL-17 17+ 群体。 IL-i 7f Li LIT 细胞已免疫 IL-17:tDI;J T 细胞 17+ 群体的发育在 DI;:JT 中受到调节，但对其如何进行了解甚少IL-17 在[ILIT 细胞中受到调节。此外，虽然在缺乏 D I;JT 细胞的小鼠中注意到缺乏 Li1;JT 反应，但已记录到对 LiT 反应的缺陷，但缺乏 LI1T 细胞的可能性，这些细胞在炎症反应早期起作用以影响启动的可能性这些启动过程还没有被探索过。我们将研究这些领域，它们对于理解探索至关重要。这些领域对于理解宿主免疫防御至关重要。防御。 -,Q” .2) =-0 0 支付 .L., E'6 --6 ，茶 0-0 小野