ASSESSING A NOVEL HYPOTHESIS THAT B-CELL ERROR CATASTROPHE CAN CAUSE GERMINAL CE
ASSESSING A NOVEL HYPOTHESIS THAT B-CELL ERROR CATASTROPHE CAN CAUSE GERMINAL CE
批准号:
8360217
负责人:
Philip John Gerrish
金额:
$5.94万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2011
资助国家:
美国
项目状态:
已结题
起止时间:
2011-06-01 至 2012-05-31
关键词:
B-LymphocytesCenters of Research ExcellenceDataDevelopmentFundingGrantImmune responseImmunoglobulin Somatic HypermutationImmunologyNational Center for Research ResourcesPopulationPrincipal InvestigatorResearchResearch InfrastructureResourcesSourceStructure of germinal center of lymph nodeTestingUnited States National Institutes of Healthcostnovelpathogensimulationtheories
中文摘要
这个子项目是许多利用资源的研究子项目之一
由NIH/NCRR资助的中心拨款提供。子项目的主要支持
而子项目的主要调查员可能是由其他来源提供的,
包括其它NIH来源。 列出的子项目总成本可能
代表子项目使用的中心基础设施的估计数量,
而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。
老年中心对于健康的免疫反应至关重要,但令人惊讶的是,人们对影响其持续或丧失的因素知之甚少。在这里,我们提出了一个新的假设,他们的损失,即体细胞超突变下的B细胞群体屈服于错误灾难的倾向。这个假设是由
最近的理论发展,从进化的角度重新推导错误突变理论。除了用大量的模拟和实验数据来验证这一假设外,我们还计划扩展我们的新理论发展,以涵盖感染性病原体和它引起的免疫反应之间的进化相互作用。
英文摘要
This subproject is one of many research subprojects utilizing the resources
provided by a Center grant funded by NIH/NCRR. Primary support for the subproject
and the subproject's principal investigator may have been provided by other sources,
including other NIH sources. The Total Cost listed for the subproject likely
represents the estimated amount of Center infrastructure utilized by the subproject,
not direct funding provided by the NCRR grant to the subproject or subproject staff.
Germinal centers are vital to a healthy immune response, yet surprisingly little is known about the factors that influence their persistence or loss. Here, we propose a novel hypothesis for their loss, namely, the propensity of B-cell populations under somatic hypermutation to succumb to error catastrophe. This hypothesis is made
possible by recent theoretical developments that re-derive error catastrophe theory from an evolutionary perspective. In addition to testing this hypothesis against extensive simulation and experimental data, we also plan to extend our new theoretical developments to encompass evolutionary interactions between an infecting pathogen and the immune response that it evokes.
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