PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 15893676

Multiple sclerosis: an immunologic perspective.

Jimmy Y Cui
View original source ↗Export metadata ↓

Abstract

The precise cause of MS remains unknown, although immunopathologic studies provide solid evidence of participation of activated immune cells in the formation of MS lesions. Cell-mediated and antibody-mediated(humoral) immune responses are involved in the immunopathogenesis of MS. The Thl and Th2 cells, by releasing a variety of pro- or anti-inflammatory cytokines, work in opposition to balance the immune response and to determine the net effect of the inflammation. The current understanding of immunopathogenesis shapes the contemporary approach to the treatment of MS. The article also reviewed the mechanisms of action of commonly used immunotherapy agents and their impact on the immune response of patients who have MS.

Explore related subjects

Antibody FormationCytokinesHumansImmunity, CellularImmunotherapyMultiple SclerosisJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Jimmy Y Cui. 2005. Multiple sclerosis: an immunologic perspective.. https://doi.org/10.1016/j.pmr.2005.01.008

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Vascular endothelial growth factor-D is a survival factor for human breast carcinoma cells.

Vascular endothelial growth factor-D (VEGF-D) stimulates growth of vascular and lymphatic endothelial cells by signaling through the tyrosine kinase receptors KDR (VEGFR-2) and Flt-4 (VEGFR-3). In the present study, we examined the effects of VEGF-D on apoptosis in human MCF-7 and MDA-MB-231 breast carcinoma cells. Because VEGF-D was not expressed constitutively in vitro, stable VEGF-D transfectants were produced. The VEGF-D-expressing MCF-7 and MDA-MB-231 lines displayed resistance to apoptosis induced by hypoxia, staurosporin and cycloheximide. Increased Bcl-2 expression, decreased homogenous caspase activities and inhibition of poly(ADP-ribose) polymerase cleavage were associated with inhibition of apoptosis in VEGF-D-expressing clones. Also, caspase-3 activation was suppressed in the VEGF-D expressing MDA-MB-231 clone. The antiapoptotic effect of VEGF-D in vitro was recapitulated in vivo using VEGF-D-expressing MDA-MB-231 xenografts. The lack of VEGFR-2 protein expression by Western blot and ineffectiveness of a neutralizing VEGFR-2 antibody in eliminating the antiapoptotic effects of VEGF-D suggest a different and yet unknown signaling mechanism. Our findings indicate that VEGF-D has a novel function as a survival factor of breast carcinoma cells in addition to its established functions as an angiogenic and lymphangiogenic factor.

Antibody Formation↗