Re: autophagy, fungi,yeast

[Guest guest]

consider fungal mimicry and how fungi have evolved ways to avoid the immune

system.

>

> 2009 Aug;7(6):743-52.

>

> Autophagy as an antimicrobial strategy.

> Subauste CS.

>

> Case Western Reserve University School of Medicine, 11100 Euclid Avenue,

Cleveland, OH 44106, USA. carlos.subauste@...

>

> Autophagy is a process of lysosomal degradation that was originally described

as a cellular response to adapt to a lack of nutrients and to enable the

elimination of damaged organelles. Autophagy is increasingly recognized as a

process that is also involved in innate and adaptive immune responses against

pathogens. Studies on the regulation of autophagy have uncovered components of

the autophagic cascade that can be manipulated pharmacologically. Approaches to

modulate autophagy may result in novel strategies for the treatment and

prevention of various infections.

>

[Guest guest]

and when I read something like this, I cant help but fell that ignorance and

ofcorse the money trail has played a hudge role in what may be the end of human

kind.

2005, 175: 6481-6488.

Copyright © 2005 by The American Association of Immunologists

Disruption of MHC Class II-Restricted Antigen Presentation by Vaccinia Virus1

Ping Li, Nan Wang, Delu Zhou, S. K. Yee, Cheong-Hee Chang, Randy R.

Brutkiewicz and Janice S. Blum2

Department of Microbiology and Immunology, Center for Immunobiology, and Walther

Oncology Center, Indiana University School of Medicine, and Walther Cancer

Institute, Indianapolis, IN 46202

Vaccinia virus (VV), currently used in humans as a live vaccine for smallpox,

can interfere with host immunity via several discrete mechanisms. In this study,

the effect of VV on MHC class II-mediated Ag presentation was investigated.

Following VV infection, the ability of professional and nonprofessional APC to

present Ag and peptides to CD4+ T cells was impaired. Viral inhibition of class

II Ag presentation could be detected within 1 h, with diminished T cell

responses dependent upon the duration of APC infection and virus titer. Exposure

of APC to replication-deficient virus also diminished class II Ag presentation.

Virus infection of APC perturbed Ag presentation by newly synthesized and

recycling class II molecules, with disruptions in both exogenous and cytoplasmic

Ag presentation. Virus-driven expression of an endogenous Ag, failed to restore

T cell responsiveness specific for this Ag in the context of MHC class II

molecules. Yet, both class II protein steady-state and cell surface expression

were not altered by VV. Biochemical and functional analysis revealed that VV

infection directly interfered with ligand binding to class II molecules.

Together, these observations suggest that disruption of MHC class II-mediated Ag

presentation may be one of multiple strategies VV has evolved to escape host

immune surveillance.

http://www.jimmunol.org/cgi/content/abstract/175/10/6481