PubMed · 14903424
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A G OSLER, J H STRAUSS, M M MAYER. 1952. Diagnostic complement fixation. I. A method.. https://pubmed.ncbi.nlm.nih.gov/14903424/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
HIV infection occurs primarily through mucosal surfaces, indicating that protection at mucosal sites may be crucial in prevention and treatment. The host innate and adaptive immune elements provide a level of protection, which differs between mucosal compartments, and appears to be most successful in the oral environment, where transmission is rare. In addition to the distinct oral mucosal architecture and cellular constituents, oral fluids, unlike other mucosal secretions, are rarely a vehicle for HIV infection. Multiple soluble factors may contribute to this antiviral activity, including neutralizing antibodies, secretory leukocyte protease inhibitor (SLPI), antiviral peptides such as defensins and cystatins, glycoproteins including thrombospondin and lactoferrin, and complement components. Understanding the antiviral activities of these and other potential resistance factors is becoming increasingly important in attempts to design treatments in the era of HAART resistance. In this regard, the mechanism of anti-HIV action of SLPI has recently been further elucidated by the discovery of its binding protein/receptor, which plays a key role in the infection of macrophages and may consequently be a novel therapeutic target. Continued elucidation of the unique features of mucosal HIV immunology is essential for understanding HIV pathogenesis and for developing effective vaccines and therapeutics.
OBJECTIVE: Little is known about the role of local production of complement components by dendritic cells (DCs) during the generation of specific immune responses. In this study, we demonstrate that human DCs are an extrahepatic source of several soluble complement proteins. METHODS: Reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot were used to evaluate the expression and production of several complement proteins. RESULTS: We show that DCs produce C3, C5, C9, Factor (F)I, FH, FB, FD and properdin at levels similar to macrophages. Treatment of DCs with lipopolysaccharide (LPS) promoted an increase in the expression of C3 and FI mRNAs and a decrease in C5 mRNA, while C9, FH, FB, FD and properdin mRNA levels were not affected. Treatment with interleukin (IL) -1 or dexamethasone induced a modest increase in C3 mRNA levels and did not affect the expression of other complement components. CONCLUSION: DCs are a source of complement proteins whose synthesis may be regulated in response to different inflammatory stimuli.
Complement activity was first described in the 1890s and the characterisation of this highly complex system has continued ever since. This review traces the history of complement research from its beginnings until it was transformed by the advent of molecular biology in the 1980s. It takes as a focus point the CIBA symposium on Complement held in London in May 1964 and reflects-and is slanted by-the views and research experience of the author.