Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement Inactivator Proteins”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources

[Mechanisms of the mediated neutrophil reactivity to Escherichia coli peptidoglycan].

The opsonic properties of normal serum with respect to E. coli peptidoglycan was studied under the actual conditions of the oxygen-dependent metabolism of neutrophils. In the course of the differentiated study of the influence of antibodies, the classical and the alternative cascades of complement the serum was heated, treated with ethylenediaminetetraacetate and ethylene glycol tetraacetate, exhausted in the cold. In serial experiments the opsonic activity of purified fibronectin was studied. The indirect reactions were shown to be the leading mechanisms of the neutrophil-stimulated activity of E. coli peptidoglycan. IgG was found to be in the center of the opsonic cooperation and thus to determine the quantitative manifestation of the total phenomenon. Complement proved to be of lesser importance; depending on the conditions of the experiment, the activation of complement occurred by the alternative way (after the removal of antibodies) or the classical way (whole serum). The actual contribution of IgG-independent and complement-independent opsonins was insignificant. Fibronectin in physiological concentrations showed no opsonic activity.

Antibodies, Bacterial↗

Evidence for an anticomplementary factor associated with human bone marrow cells.

Complement (C)-mediated lysis of antibody-sensitized sheep erythrocytes was inhibited by the addition of human bone marrow cells. The anticomplementary activity could be attributed to a soluble factor that was released from the bone marrow cells. This factor inhibited at an early stage in the C-cascade and showed the characteristics of a factor that accelerates decay of C2. The release of such a factor by bone marrow cells would present an obstacle to the use of antibody and C to purge tumor cells from bone marrow that is to be used for autologous transplantation.

Animals↗

[Nonspecific immunity factors and elimination of circulating immune complexes in patients with myocardial infarct in the 1st phase of rehabilitation].

A considerable increment of humoral immunity parameters was demonstrated during the 3d-5th week after the onset of myocardial infarction (MI). The levels of IgG and IgE were increased, and those of circulating immune complexes (CIC), decreased significantly in patients with their first diagnosed infarction, as compared to those with repeated MI. Patients with repeated MI showed significantly reduced blood C3c, C4 and the phagocyte index in the presence of high blood levels of CIC and C-reactive protein, as compared to patients with primary infarction. The results are indicative of a considerable activation of the complement and the phagocytic system and CIC elimination in patients with their first MI diagnosis, and the absence of such a stimulation in repeated MI cases.

Adult↗