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Antimicrobial mechanisms in response to Mycobaterium leprae infection.

紀錄類型:	書目-電子資源 : Monograph/item
書名/作者:	Antimicrobial mechanisms in response to Mycobaterium leprae infection.
作者:	Dang, Angeline Tilly.
出版者:	Ann Arbor : : ProQuest Dissertations & Theses, , 2016
面頁冊數:	132 p.
附註:	Source: Dissertation Abstracts International, Volume: 77-10(E), Section: B.
Contained By:	Dissertation Abstracts International77-10B(E).
標題:	Immunology.
ISBN:	9781339835853
摘要、提要註:	The human body is constantly exposed to a myriad of bacterial organisms, and in most cases, colonization of the host by these commensal bacteria is harmless and may even be beneficial. However, a subset of bacteria are pathogenic causing debilitating health that can lead to fatal diseases. Many microbes deploy strategies to evade and impair the host response, further contributing to disease severity. In response to infectious agents, the host can control and subvert infections by triggering both innate and adaptive immunity. The microenvironment in which an infections occurs greatly dictates the strength, quality, and duration of immune responses. Herein, we demonstrate mechanisms for triggering protective immune responses during Mycobacterium leprae infection. Specifically, treatment of M. leprae-infected CD1a+ Langerhans cells, a dendritic cells subset localized in the skin and mucosa, with IFN-gamma induces autophagy, leading to increased antimicrobial activity and antigen presentation to T cells. Furthermore, T cells secrete elevated amounts of IFN-gamma following antigenic activation, providing an amplification loop to further augment effective host immunity. As M. leprae predominantly infect and reside in macrophages, we also investigated mechanisms of macrophage activation. Our data reveals that treatment of M. leprae-infected monocyte-derived-macrophages with IL-26, a T cell cytokine, results in reduced viability of intracellular bacteria. IL-26 may have dual roles in antimycobacterial defense, one which involves binding to bacterial bacilli and directly reducing its viability; and the other involving activation of infected macrophages, increasing bacterial traffic to the lysosomes, where they are degraded.

Antimicrobial mechanisms in response to Mycobaterium leprae infection.
Dang, Angeline Tilly.

Antimicrobial mechanisms in response to Mycobaterium leprae infection. - Ann Arbor : ProQuest Dissertations & Theses, 2016 - 132 p.

Source: Dissertation Abstracts International, Volume: 77-10(E), Section: B.

Thesis (Ph.D.)--University of California, Los Angeles, 2016.

The human body is constantly exposed to a myriad of bacterial organisms, and in most cases, colonization of the host by these commensal bacteria is harmless and may even be beneficial. However, a subset of bacteria are pathogenic causing debilitating health that can lead to fatal diseases. Many microbes deploy strategies to evade and impair the host response, further contributing to disease severity. In response to infectious agents, the host can control and subvert infections by triggering both innate and adaptive immunity. The microenvironment in which an infections occurs greatly dictates the strength, quality, and duration of immune responses. Herein, we demonstrate mechanisms for triggering protective immune responses during Mycobacterium leprae infection. Specifically, treatment of M. leprae-infected CD1a+ Langerhans cells, a dendritic cells subset localized in the skin and mucosa, with IFN-gamma induces autophagy, leading to increased antimicrobial activity and antigen presentation to T cells. Furthermore, T cells secrete elevated amounts of IFN-gamma following antigenic activation, providing an amplification loop to further augment effective host immunity. As M. leprae predominantly infect and reside in macrophages, we also investigated mechanisms of macrophage activation. Our data reveals that treatment of M. leprae-infected monocyte-derived-macrophages with IL-26, a T cell cytokine, results in reduced viability of intracellular bacteria. IL-26 may have dual roles in antimycobacterial defense, one which involves binding to bacterial bacilli and directly reducing its viability; and the other involving activation of infected macrophages, increasing bacterial traffic to the lysosomes, where they are degraded.

ISBN: 9781339835853Subjects--Topical Terms:

402223
Immunology.

Antimicrobial mechanisms in response to Mycobaterium leprae infection.
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