properdin


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properdin

 [pro´per-din]
a protein of the alternative complement pathway, augmenting complement activation. Called also factor P.

pro·per·din

(prō'per-din),
A control protein for the alternate complement cascade, properdin stabilizes the C3 convertase enzyme, a deficiency of which increases susceptibility to systemic meningococcal infections and can be inherited in an x-linked pattern.
See also: properdin system, component of complement, factor P.
[pro- + L. perdo, to destroy]

properdin

(prō-pûr′dn)
n.
A protein in blood serum that is a component of the innate immune system, acting as a positive regulator of the alternative pathway of the complement system.

pro·per·din

(prō'pĕr-din)
A group of proteins involved in resistance to infection that participate, in conjunction with other factors, in an alternate pathway to the activation of the terminal components of complement.
See also: properdin system, component of complement
[pro- + L. perdo, to destroy]
References in periodicals archive ?
In Table 4, complement C3, complement C4, complement component C6, complement factor H precursor, properdin precursor, complement component C8 gamma chain, complement component C8 beta chain, adiponectin, galectins, fibronectin type III domain-containing protein 1, fibrinogen beta chain, fibrinogen gamma chain, kininogen1, apolipoprotein H, and glutathione-S-transferase were included.
Van Der Pol et al., "Identification of tubular heparan sulfate as a docking platform for the alternative complement component properdin in proteinuric renal disease," Journal of Biological Chemistry, vol.
The normal levels of plasma C1q, properdin, Bb, C4BP, factor H, and C3 were 61.96 [+ or -] 10.50 [micro]g/mL, 22.58 [+ or -] 9.67 [micro]g/mL, 0.69 [+ or -] 0.45 [micro]g/mL, 326.59 [+ or -] 87.25 [micro]g/mL, 515.04 [+ or -] 134.08 [micro]g/mL, and 0.80 [+ or -] 0.17mg/mL, respectively.
TABLE Patients at high risk for meningococcal disease * Individuals with persistent complement component deficiency, such as C5-C9, properdin, or factor D * People with functional or anatomical asplenia * Microbiologists working with Neisseria meningitidis * Travelers to, or residents of, countries where meningococcal disease is hyperendemic or epidemic Source: CDC.
Kompleman sisteminin gec komponentlerinden olan C5-C9 eksikliginde meningokoklar ile rekurren menenjit gelisimi bilinirken, properdin eksikliginde meningokokkal menenjitler daha yuksek mortalite ile seyretmektedir.
* Infants with complement component deficiencies such as C3, C5-9, properdin, factor H, and factor D deficiencies.
They discuss such topics as B cell signaling and fate decision; immune function control; the molecular components, geometry, and timing of T cell activation and synapse formation; the influence of bacterial carbohydrates on the adaptive immune system; new findings on properdin and the role in inflammatory and autoimmune diseases; allergy vaccines based on allergen structures; adaptive immune regulation in the gastrointestinal tract; the acute inflammatory response and sterile stimuli; the role of antibodies in HIV vaccines; and functions of notch signaling in the immune system.
(18) In May 2007, NACI recommended the use of the quadrivalent meningococcal vaccine for immunization of persons 2-55 years in the following high-risk groups: persons with anatomic or functional asplenia; persons who have complement, properdin, or factor D deficiencies; travelers when meningococcal vaccine is indicated, including pilgrims to the Hajj in Mecca; research, industrial, and clinical laboratory personnel who are routinely exposed to N.
It also increases properdin levels, which accounts for its antibiotic effects.
This study indicates that a combined deficiency of both properdin and MBL increases the risk of infection with N.
Gliatech is developing therapeutic antibodies to properdin as potential treatments for acute inflammatory conditions which result from cardiopulmonary bypass surgery, heart attacks and stroke.
ACIP has previously recommended routine vaccination of persons aged [greater than or equal to] 2 months who have certain medical conditions that increase risk for meningococcal disease (1), including persons who have persistent (e.g., genetic) deficiencies in the complement pathway (e.g., C3, properdin, Factor D, Factor H, or C5-C9); persons receiving eculizumab (Soliris, Alexion Pharmaceuticals) for treatment of atypical hemolytic uremic syndrome or paroxysmal nocturnal hemoglobinuria (because the drug binds C5 and inhibits the terminal complement pathway); and persons with functional or anatomic asplenia (including persons with sickle cell disease).