Mechanisms of Immune Modulation and Peridontal Disease
免疫调节与牙周疾病的机制
基本信息
- 批准号:6361859
- 负责人:
- 金额:$ 29.06万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2001
- 资助国家:美国
- 起止时间:2001-09-01 至 2006-06-30
- 项目状态:已结题
- 来源:
- 关键词:B cell lymphoma Bacteroides gingivalis CD40 molecule SDS polyacrylamide gel electrophoresis bacteria infection mechanism bacterial antigens bacterial genetics cellular immunity cholera toxin cytokine enzyme linked immunosorbent assay flow cytometry gene expression immunization immunogenetics immunoglobulin G immunomodulators immunoregulation laboratory mouse monoclonal antibody mucosal immunity pathologic process periodontium disorder phospholipids surface antigens western blottings
项目摘要
Periodontal disease is the result of the host response to
periodontal pathogens such as Porphyromonas gingivalis. P. gingivalis is a
black-pigmented, Gram-negative pathogen, which expresses various virulence
factors implicated in disease. The overall goal of this project is to define
the cellular mechanism(s) involved in the induction of host responses
protective against P. gingivalis infection. The studies proposed will
concentrate on delineating the mechanisms by which adjuvants modulate host
responses to P. gingivalis antigens. Emphasis will be placed on the role of B7
co-stimulatory molecules in host responses and in infection by P. gingivalis,
and on the involvement of cytokines, specific target cells, and other cell
surface receptors. Specifically, there are plans to: 1) Determine the
immunogenicity of the recombinant catalytic domain of the lysine-specific
protease Kgp (rKgp-CAT) and the HagA repeat domain (rHArep) of P. gingivalis,
and the effect of the B subunit of cholera toxin (CTB) and monophosphoryl lipid
A (MPL) in modulating responses to these antigens following intranasal
immunization, The level, isotype and IgG subclass of antibodies induced to
HArep or Kgp-CAT in serum and external secretion$ will be measured by ELISA.
The effects of CTB and MPL in enhancing/shifting responses will be further
characterized by measuring antigen-specific proliferation and cytokine
production. The effect of the responses, especially the nature of the
antibodies, on protection will also be determined. 2) Determine the mechanisms
by which the adjuvants CTB and MPL modulate the induction of the immune
response. These studies will determine the involvement of the co-stimulatory B7
molecules in the immunoenhancing ability of the adjuvants and in P. gingivalis
infection, the target cells affected by the adjuvants and the association
between MPL, the Toll-like receptors and B7 co-stimulatory molecules. Groups of
mice deficient in B7-l (B7-1-/-), B7-2 (B7-2j or both (B7-1/B7-2-/-) molecules
and normal controls will be immunized with HArep or Kgp-CAT with and without
CTB or MIPL. The levels of antibody and antibody-secreting cells will be
assessed by ELISA and ELISPOT method. The effect of adjuvants on the expression
of B7 molecules and of CD4OL will be analyzed by FACS. Differential regulation
of cytokines induced and proliferative responses will also be assessed. The
involvement of B7 co-stimulation in P. gingivalis infection will be assessed in
B7 deficient mice. These studies will provide information on the mechanisms by
which mucosal adjuvants modulate host immune responses, the target cells
through which their adjuvanticity is exerted and the involvement of
co-stimulatory signals provided by B7 molecules and of Toll-like receptors. An
understanding of these processes is crucial for the development of means to
interrupt/prevent periodontal disease pathogenesis by Porphyromonas gingivalis.
Knowledge on the host effects induced by a potential periodontal vaccine will
lead to the development of the therapeutic manipulation of effector function
leading to the amelioration or prevention of periodontal disease and associated
systemic diseases.
牙周病是宿主对牙周病反应的结果
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Jannet Katz其他文献
Jannet Katz的其他文献
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{{ truncateString('Jannet Katz', 18)}}的其他基金
Mechanisms of Immune Modulation and Peridontal Disease
免疫调节与牙周疾病的机制
- 批准号:
6516680 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
7422575 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
6606156 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
7568853 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
7380161 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
8089431 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
6760213 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
7851438 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
Mechanisms of Immune Modulation and Periodontal Disease
免疫调节与牙周病的机制
- 批准号:
6884589 - 财政年份:2001
- 资助金额:
$ 29.06万 - 项目类别:
MECHANISM(S) OF PROPHYROMONAS GINGIVALIS ADHERENCE
牙龈卟啉单胞菌的粘附机制
- 批准号:
6011653 - 财政年份:1999
- 资助金额:
$ 29.06万 - 项目类别:
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