|1.||Yan, Jun: 6 articles (06/2013 - 12/2003)|
|2.||Ross, Gordon D: 3 articles (06/2005 - 12/2003)|
|3.||Baran, Jarek T: 3 articles (06/2005 - 12/2003)|
|4.||Allendorf, Daniel J: 3 articles (06/2005 - 12/2003)|
|5.||Hansen, Richard D: 3 articles (06/2005 - 12/2003)|
|6.||Cheung, Nai-Kong V: 3 articles (06/2005 - 05/2002)|
|7.||Tsokos, George C: 2 articles (05/2014 - 09/2005)|
|8.||Harris, Claire L: 2 articles (01/2014 - 08/2011)|
|9.||Neal, James W: 2 articles (01/2014 - 01/2012)|
|10.||Morgan, B Paul: 2 articles (01/2014 - 01/2012)|
11/01/2014 - "CRIg-L-FH, slightly more potent than CRIg-FH, considerably inhibited both AP- and also classical pathway (CP)-mediated hemolysis and successfully eliminated the deposition of C3b/iC3b. "
03/18/2010 - "With a goal of improving PNH therapy, we characterized the activity of anti-C3b/iC3b monoclonal antibody 3E7 in an in vitro model of APC-mediated hemolysis. "
01/01/2013 - "More intriguingly, a human fusion protein consisting of the iC3b/ C3d-binding region of complement receptor 2 and of the inhibitory domain of the CAP regulator factor H has been recently shown effective in inhibiting, in vitro, both intravascular hemolysis of and surface C3-deposition on PNH erythrocytes, and is now under investigation in phase 1 clinical trials."
02/01/2013 - "Complement component 3b (C3b), a marker of acute inflammation, was not significantly altered. "
11/22/2011 - "We establish herein that cell contact-mediated nTreg regulatory function is inhibited by inflammation, especially in the presence of the complement C3b receptor (CD46). "
08/15/1994 - "Disseminated (DGI) isolates typically resist killing by normal serum (are serum-resistant), inactivate more C3b (to iC3b preferentially bound via amide linkages), generate less C5a, and result in less inflammation at local sites. "
08/09/2011 - "iC3b then interacts with the complement receptors (CR) of the Ig superfamily, CR2 (CD21), CR3 (CD11b/CD18), and CR4 (CD11c/CD18) on leukocytes, down-modulating inflammation, enhancing B cell-mediated immunity, and targeting pathogens for clearance by phagocytosis. "
05/01/1996 - "The deposition was enhanced in relation to the severity of mucosal inflammation (C3b, P less than 0.05; iC3b/C3dg, P less than 0.01). "
|4.||Systemic Lupus Erythematosus (Libman-Sacks Disease)
12/01/2009 - "Impaired C3b/iC3b deposition on Streptococcus pneumoniae in serum from patients with systemic lupus erythematosus."
10/14/1982 - "The erythrocytes of patients with systemic lupus erythematosus have been shown to have a decreased number of receptors for the major cleavage fragment of the third component of complement (C3b). "
01/01/1990 - "Seventy-one patients with systemic lupus erythematosus (SLE), seen in an outpatient setting for follow-up evaluation during a 3-mo period, were tested (in addition to routine lupus monitoring studies) with enzyme immunoassays (EIAs) for anti-DNA, iC3b, and factor Bb to determine the relationship of these test results to disease activity. "
03/01/1987 - "Studies on human blood lymphocytes with iC3b (type 3) complement receptors: III. Abnormalities in patients with active systemic lupus erythematosus."
11/01/1994 - "The expression of Fc gamma RI, Fc gamma RII, and Fc gamma RIII (the IgG receptors CD64, CD32, CD16) as well as CR3 (the C3bi receptor, CD11b) on monocytes in the blood of patients with systemic lupus erythematosus (SLE) was investigated. "
06/01/1988 - "In contrast, burn patient neutrophils expressed normal levels of class I HLA molecules and the C3bi receptor. "
08/01/1999 - "Flow cytometric analysis (FCM) was used to study PMLs expression of IgG Fc-receptor III (Fc gamma RIII) as well as the complement receptors CR1 (receptor for C3b) and CR3 (receptor for C3bi) in 23 patients with large burns. "
02/01/1994 - "We have used flow cytometric analysis (FCM) to longitudinally study PMNL expression of IgG Fc-receptor II (Fc gamma RII) and Fc-receptor III (Fc gamma RIII), as well as the complement receptors CR1 (receptor for C3b) and CR3 (receptor for C3bi) in 22 patients with large burns. "
|2.||Complement System Proteins (Complement)
|3.||Complement Factor H (Factor H)
|4.||Complement 3d Receptors (Complement Receptor 2)
|5.||von Willebrand Factor
|6.||Complement Receptors (Complement Receptor)
|7.||Fc Receptors (Fc Receptor)
|8.||Immunoglobulin G (IgG)
|9.||Macrophage-1 Antigen (Macrophage 1 Antigen)
|10.||IgG Receptors (Fc gamma RI)
|1.||Homologous Transplantation (Allograft)
|2.||Renal Dialysis (Hemodialysis)