PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6978365

In vitro complement activation by intercellular antibodies.

T Hashimoto·M Sugiura·S Kurihara·T Nishikawa
View original source ↗Export metadata ↓

Abstract

By in vitro complement immunofluorescence, 6 sera from pemphigus with intercellular antibodies were tested for their capability to fix C1q, C4, C3, and properdin. All 6 serum samples yielded positive reaction for C3 staining. Three serum samples gave positive staining for C1q, 5 serum samples for C4, and 3 serum samples for properdin, respectively. Substitution of C2 deficient serum as a complement source inhibited C3 and properdin staining but not positive C1q and C4 staining. These results are best explained by the concept that complement activation in vitro by intercellular antibodies occurs via the classical pathway followed by assembly of the C3 amplification mechanism.

Explore related subjects

AntibodiesComplement Activating EnzymesComplement ActivationComplement C1qComplement C3Complement C4HumansImmunoglobulin GPemphigusProperdinSkinJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T Hashimoto, M Sugiura, S Kurihara, T Nishikawa. 1982. In vitro complement activation by intercellular antibodies.. https://doi.org/10.1111/1523-1747.ep12507396

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

KEEP EXPLORING

Related citations

PubMed2021

ERBB3 overexpression due to miR-205 inactivation confers sensitivity to FGF, metabolic activation, and liability to ERBB3 targeting in glioblastoma.

In glioblastoma (GBM), the most frequent and lethal brain tumor, therapies suppressing recurrently altered signaling pathways failed to extend survival. However, in patient subsets, specific genetic lesions can confer sensitivity to targeted agents. By exploiting an integrated model based on patient-derived stem-like cells, faithfully recapitulating the original GBMs in vitro and in vivo, here, we identify a human GBM subset (∼9% of all GBMs) characterized by ERBB3 overexpression and nuclear accumulation. ERBB3 overexpression is driven by inheritable promoter methylation or post-transcriptional silencing of the oncosuppressor miR-205 and sustains the malignant phenotype. Overexpressed ERBB3 behaves as a specific signaling platform for fibroblast growth factor receptor (FGFR), driving PI3K/AKT/mTOR pathway hyperactivation, and overall metabolic upregulation. As a result, ERBB3 inhibition by specific antibodies is lethal for GBM stem-like cells and xenotransplants. These findings highlight a subset of patients eligible for ERBB3-targeted therapy.

Antibodies↗