𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Activation of the classical pathway of complement by rheumatoid factors

✍ Scribed by Umesh K. Sabharwal; John H. Vaughan; Sherman Fong; Peter H. Bennett; Dennis A. Carson; John G. Curd


Publisher
John Wiley and Sons
Year
1982
Tongue
English
Weight
667 KB
Volume
25
Category
Article
ISSN
0004-3591

No coin nor oath required. For personal study only.

✦ Synopsis


Abstract

A simple, sensitive solid‐phase radioimmunoassay to quantitate the activation of the classical pathway of complement by rheumatoid factor (RF) is described. RF (purified, in serum or synovial fluid) was bound to reduced and alkylated IgG adsorbed to polyvinyl chloride microtiter plates and reacted with diluted normal human serum (complement). The activation and binding of C4 were quantitated with ^125^I‐Fab'~2~‐anti‐C4. Purified, polyclonal IgM–RF was 100‐ to 1,000‐fold more effective than purified IgG–RF in activating complement. The amount of complement activation produced by RF in each of the 57 sera and 2 synovial fluid samples correlated directly with the amount of IgM–RF present. The complement activating abilities of polyclonal IgM–RF in the sera of 15 rheumatoid arthritis patients were homogeneous. This novel technique is readily applicable to the investigation of complement activation by RF in disease.


📜 SIMILAR VOLUMES


C1q, the recognition subcomponent of the
✍ Katrin Färber; Giselle Cheung; Daniel Mitchell; Russell Wallis; Eberhard Weihe; 📂 Article 📅 2009 🏛 John Wiley and Sons 🌐 English ⚖ 332 KB

## Abstract Microglia, central nervous system (CNS) resident phagocytic cells, persistently police the integrity of CNS tissue and respond to any kind of damage or pathophysiological changes. These cells sense and rapidly respond to danger and inflammatory signals by changing their cell morphology;

Complement activation by both classical
✍ Max Albert Hietala; Kutty S Nandakumar; Linda Persson; Susann Fahlén; Rikard Hol 📂 Article 📅 2004 🏛 John Wiley and Sons 🌐 English ⚖ 327 KB

## Abstract To analyze the role of the classical and alternative pathways of complement activation in the effector phase of arthritis, we have induced arthritis in C3‐ and factor B (FB)‐deficient (C3^–/–^ and FB^–/–^) DBA/1J mice using well‐defined monoclonal IgG2b and IgG2a antibodies to type II c