CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity.

CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity. Research Abstract Details 

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CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity. Abstract Text:

Kei Kawana,Alison J Quayle,Mercedes Ficarra,Joyce A Ibana,Li Shen,Yukiko Kawana,Huixia Yang,Luis Marrero,Sujata Yavagal,Sheila J Greene,You-Xun Zhang,Richard B Pyles,Richard S Blumberg,Danny J Schust,

Chlamydia trachomatis is an obligate intracellular pathogen that can persist in the urogenital tract. Mechanisms by which C. trachomatis evades clearance by host innate immune responses are poorly described. CD1d is MHC-like, is expressed by epithelial cells, and can signal innate immune responses by NK and NKT cells. Here we demonstrate that C. trachomatis infection down-regulates surface-expressed CD1d in human penile urethral epithelial cells through proteasomal degradation. A chlamydial proteasome-like activity factor (CPAF) interacts with the CD1d heavy chain, and CPAF-associated CD1d heavy chain is then ubiquitinated and directed along two distinct proteolytic pathways. The degradation of immature glycosylated CD1d was blocked by the proteasome inhibitor lactacystin but not by MG132, indicating that degradation was not via the conventional proteasome. In contrast, the degradation of non-glycosylated CD1d was blocked by lactacystin and MG132, consistent with conventional cellular cytosolic degradation of N-linked glycoproteins. Immunofluorescent microscopy confirmed the interruption of CD1d trafficking to the cell surface, and the dislocation of CD1d heavy chains into both the cellular cytosol and the chlamydial inclusion along with cytosolic CPAF. C. trachomatis targeted CD1d toward two distinct proteolytic pathways. Decreased CD1d surface expression may help C. trachomatis evade detection by innate immune cells and may promote C. trachomatis persistence.

CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity. Publishing Authors By Initials

K Kawana,AJ Quayle,M Ficarra,JA Ibana,L Shen,Y Kawana,H Yang,L Marrero,S Yavagal,SJ Greene,YX Zhang,RB Pyles,RS Blumberg,DJ Schust,

For similar macromolecular substances: multiprotein complexes: multienzyme complexes: proteasome endopeptidase complex research abstracts see: macromolecular substances: multiprotein complexes: multienzyme complexes: proteasome endopeptidase complex research

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CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of biological chemistry

VOLUME: 282

Page Numbers: 7368-75

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 10

MONTH: 01

YEAR: 2007

CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity. Information

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LANGUAGE: eng

NlmUniqueID: 2985121

CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity. Keywords Mesh Terms:

KEYWORDS: Proteasome Endopeptidase Complex

MESH TERMS: metabolism

Chemical & Substance for Abstract: CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity. Information

Substance Name: Proteasome Endopeptidase Complex

Registry Number: EC 3.4.25.1

Grant and Affiliation Information for CD1d degradation in Chlamydia trachomatis-infected epithelial cells is the result of both cellular and chlamydial proteasomal activity.

AFFILIATION: Division of Reproductive Biology, Department of Obstetrics and Gynecology, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts 02118.

Country: United States

AGENCY: United States NIAID

GRANT: U19AI061972

ACRONYM: AI

MEDLINETA: J Biol Chem

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