The HLA class III region is formed by genes that code components of the complement pathway (C2,
properdin, factor B, C4A, and C4B) and products with inflammatory activity such as TNF-[alpha] and acute phase proteins [25].
* Persons with persistent complement component deficiencies (including inherited or chronic deficiencies in C3, C5-C9,
properdin, factor D, factor H, or who are taking eculizumab [Solaris]); persons with anatomic or functional asplenia (including sickle cell disease); microbiologists routinely exposed to isolates of Neisseria meningitidis; persons identified as at increased risk because of a serogroup B meningococcal disease outbreak.
In the alternative complement pathway, C3b reacts with the proteins factor B, adipsin, and
properdin to compose C3 convertase.
[64.] Morrison DC, Kline LF (1977) Activation of the classical and
properdin pathways of complement by bacterial lipopolysaccharides (LPS).
(10) This could be due to decreased serum immunoglobulin, protein deficiency, decreased bactericidal activity of the leukocytes, immunosuppressive therapy, decreased perfusion of the spleen caused by hypovolemia and loss in the urine of a complement factor (
Properdin factor 3) that opsonizes certain bacteria.
Involvement of the classic and alternate (
properdin) pathways for complement activation.
Plasma concentrations of major human complement components were determined by enzyme-linked immunoassays, including complement fragments C5a (Quidel Corporation, San Diego, CA), C3a (Quidel Corporation, San Diego, CA), Bb (Quidel Corporation, San Diego, CA), soluble C5b-9 (SC5b-9, Quidel Corporation, San Diego, CA),
properdin (Uscnk Life Science Inc., Wuhan, China), and C3 (Quidel Corporation, San Diego, CA).
Stover, "The role of
properdin in murine zymosan-induced arthritis," Molecular Immunology, vol.
The hyalinotic lesions are usually formed by nonspecific trapping of the high-molecular-weight circulating proteins, such as IgM and C1q, and these lesions must be distinguished from the immune-complex deposits seen in other forms of glomerular diseases, where additional components of the complement, that is, C3 and
properdin, also display reactivity in these deposits.
Naked and poloxamine-coated nanoparticles in the mushroom and mushroom-brush conformation also activate the complement through the alternative pathway by covalent conjugation of
properdin to poloxamine and the C3 component adsorption.