Processing of Mycobacterium tuberculosis antigen 85B involves intraphagosomal formation of peptide-major histocompatibility complex II complexes and is inhibited by live bacilli that decrease phagosome maturation.
Processing of Mycobacterium tuberculosis antigen 85B involves intraphagosomal formation of peptide-major histocompatibility complex II complexes and is inhibited by live bacilli that decrease phagosome maturation.
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DOI:
10.1084/jem.194.10.1421
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发表时间:
2001-11-19
期刊:
影响因子:
--
通讯作者:
Harding CV
中科院分区:
文献类型:
--
作者:
Ramachandra L;Noss E;Boom WH;Harding CV
Mycobacterium tuberculosis (MTB) inhibits phagosomal maturation to promote its survival inside macrophages. Control of MTB infection requires CD4 T cell responses and major histocompatibility complex (MHC) class II (MHC-II) processing of MTB antigens (Ags). To investigate phagosomal processing of MTB Ags, phagosomes containing heat-killed (HK) or live MTB were purified from interferon-γ (IFN-γ)–activated macrophages by differential centrifugation and Percoll density gradient subcellular fractionation. Flow organellometry and Western blot analysis showed that MTB phagosomes acquired lysosome-associated membrane protein-1 (LAMP-1), MHC-II, and H2-DM. T hybridoma cells were used to detect MTB Ag 85B(241–256)–I-Ab complexes in isolated phagosomes and other subcellular fractions. These complexes appeared initially (within 20 min) in phagosomes and subsequently (>20 min) on the plasma membrane, but never within late endocytic compartments. Macrophages processed HK MTB more rapidly and efficiently than live MTB; phagosomes containing live MTB expressed fewer Ag 85B(241–256)–I-Ab complexes than phagosomes containing HK MTB. This is the first study of bacterial Ag processing to directly show that peptide–MHC-II complexes are formed within phagosomes and not after export of bacterial Ags from phagosomes to endocytic Ag processing compartments. Live MTB can alter phagosome maturation and decrease MHC-II Ag processing, providing a mechanism for MTB to evade immune surveillance and enhance its survival within the host.
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影响因子:
3.1
作者:
HAVLIR, DV;WALLIS, RS;ELLNER, JJ
通讯作者:
ELLNER, JJ
影响因子:
64.8
作者:
PETERS, PJ;NEEFJES, JJ;GEUZE, HJ
通讯作者:
GEUZE, HJ
影响因子:
7.8
作者:
Kleijmeer, MJ;Morkowski, S;Geuze, HJ
通讯作者:
Geuze, HJ
影响因子:
15.3
作者:
Clemens, DL;Horwitz, MA
通讯作者:
Horwitz, MA
影响因子:
5.4
作者:
HARDING, CV
通讯作者:
HARDING, CV