The Danger Model 2: how tissues control Immunity

危险模型 2：组织如何控制免疫力

• 批准号: 10932746
• 负责人: POLLY C MATZINGER
• 金额: $ 16.29万
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10932746
• 关键词: Adult; Area; Autoimmune Responses; Autoimmunity; Cells; Chicago; Collaborations; Communication; Development; Education; Genes; Health; Immune; Immune response; Immune system; Immunity; Immunoglobulin A; Immunologist; Infection; Intestines; Malignant Neoplasms; Modeling; Mus; National Institute of Allergy and Infectious Disease; Natural regeneration; Neonatal; Organism; Parasitology; Research; Scientist; Signal Transduction; System; T-Lymphocyte; Testing; Thymus Gland; Tissues; Transplantation; Universities; Vaccines; Virus Diseases; fighting; healing; humoral immunity deficiency; immunoreaction; infancy; intestinal epithelium; neonate; pathogen; response

Because our lab was shut down by the NIAID administration on April 1st, 2013, we focused on three projects that had some possibility of completion. We managed to finish one of these projects, but will continue the others through collaborations with other scientists on and off campus. Ongoing projects from the Ghost Lab 1) (Collaboration with Bana Jabri, University of Chicago). IgA and B cell deficient mice show changes in intestinal epithelium indicating that these cells take up several aspects of immunity. Most of these changes only occur when the intestines harbor commensal organisms. we are now ascertaining which of the these commensals are responsible for stimulating the innate immune genes in the intestinal epithelium.

由于我们的实验室在2013年4月1日被NIAID政府关闭，因此我们专注于三个有可能完成的项目。 我们设法完成了其中一个项目，但将通过与校园内外的其他科学家的合作来继续其他项目。 幽灵实验室正在进行的项目 1）（与芝加哥大学Bana Jabri合作）。 Iga和B细胞缺乏小鼠显示肠上皮的变化，表明这些细胞占据了免疫的几个方面。 这些变化大多数只有在肠道具有共生生物时才发生。 我们现在正在确定哪些共生负责刺激肠上皮中的先天免疫基因。

项目成果

Transient autoantibodies to danger signals.

• DOI: 10.3389/fimmu.2023.1046300
• 发表时间: 2023
• 期刊: FRONTIERS IN IMMUNOLOGY
• 影响因子: 7.3
• 作者: Shaw, Elana R.;Matzinger, Polly
• 通讯作者: Matzinger, Polly

Spontaneous mutation in the Cd79b gene leads to a block in B-lymphocyte development at the C' (early pre-B) stage.

• DOI: 10.1038/gene.2009.70
• 发表时间: 2009-12
• 期刊: GENES AND IMMUNITY
• 影响因子: 5
• 作者: Shulzhenko, N.;Morgun, A.;Matzinger, P.
• 通讯作者: Matzinger, P.

Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cells.

• DOI: 10.1038/ni.1695
• 发表时间: 2009-02
• 期刊: Nature immunology
• 影响因子: 30.5

The evolution of the danger theory. Interview by Lauren Constable, Commissioning Editor.

• DOI: 10.1586/eci.12.21
• 发表时间: 2012-05
• 期刊: Expert review of clinical immunology
• 影响因子: 4.4
• 作者: Matzinger P

Protective response to Leishmania major in BALB/c mice requires antigen processing in the absence of DM.

• DOI: 10.4049/jimmunol.0803956
• 发表时间: 2009-04-15
• 期刊: Journal of immunology (Baltimore, Md. : 1950)
• 作者: Kamala T;Nanda NK
• 通讯作者: Nanda NK