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Innate immunity: Receptors and effe...
~
Ramanathan, Balaji.
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Innate immunity: Receptors and effectors.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Innate immunity: Receptors and effectors./
作者:
Ramanathan, Balaji.
面頁冊數:
157 p.
附註:
Source: Dissertation Abstracts International, Volume: 65-07, Section: B, page: 3249.
Contained By:
Dissertation Abstracts International65-07B.
標題:
Biology, Animal Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3140161
ISBN:
0496873029
Innate immunity: Receptors and effectors.
Ramanathan, Balaji.
Innate immunity: Receptors and effectors.
- 157 p.
Source: Dissertation Abstracts International, Volume: 65-07, Section: B, page: 3249.
Thesis (Ph.D.)--Kansas State University, 2004.
One component of immunity, the phylogenetically ancient innate immune response, fights infection from the moment of first contact and is the fundamental defensive weapon of multicellular organisms. We chose three aspects of innate immunity to study the role of innate immunity in host defense.
ISBN: 0496873029Subjects--Topical Terms:
1017835
Biology, Animal Physiology.
Innate immunity: Receptors and effectors.
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Source: Dissertation Abstracts International, Volume: 65-07, Section: B, page: 3249.
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Major Professor: Frank Blecha.
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Thesis (Ph.D.)--Kansas State University, 2004.
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One component of immunity, the phylogenetically ancient innate immune response, fights infection from the moment of first contact and is the fundamental defensive weapon of multicellular organisms. We chose three aspects of innate immunity to study the role of innate immunity in host defense.
520
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In the first investigation, we cloned and characterized the cDNA for porcine triggering receptors expressed on myeloid cells-1 (pTREM-1) from bone marrow cells that predicts a 238 amino-acid peptide. pTREM-1 mRNA was expressed in several tissues. In vitro and in vivo studies showed upregulation of gene expression indicating a role in recognition of microorganisms. These findings provide fundamental comparative data indicating that bacterial infection induces TREM-1 expression.
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In the second study, we investigated a novel activity of PR-39, a porcine antimicrobial peptide. PR-39 altered macrophage viability by inhibiting apoptosis, which was induced by nutrient depletion, LPS stimulation or camptothecin treatment. This antiapoptotic effect was significant and was associated with a decrease in caspase-3 activity. These findings suggest that PR-39 might function in the inflammatory milieu not only to kill bacteria, but also to aid in modulating the viability of inflammatory cells by regulating apoptosis.
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The third study explored gene regulation of prophenin-2, a 97-amino-acid porcine antimicrobial protein. In this study, we characterized the 5 ' regulatory regions of the PF-2 gene to understand the molecular mechanisms regulating its expression. Using a bioinformatics approach to identify several potential transcription factor binding sites, site-directed mutagenesis and transactivation experiments, we found that the PF-2 gene was regulated by PU.1 and MZF-1 and by cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3). Taken together, these results identify cis- and trans-acting factors involved in the regulation of PF-2 and clarify mechanisms of cathelidicin gene regulation.
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In summary, these investigations provide a better insight into innate immune mechanisms in terms of pathogen recognition (TREM-1), effector molecules (PR-39) and gene regulation (PF-2).
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