Results 61 to 70 of about 70,452 (309)

Engineering novel complement activity into a pulmonary surfactant protein [PDF]

open access: yes, 2010
Complement neutralizes invading pathogens, stimulates inflammatory and adaptive immune responses, and targets non- or altered-self structures for clearance.
Anthony H. Keeble   +38 more
core   +2 more sources

ApoE attenuates unresolvable inflammation by complex formation with activated C1q

open access: yesNature Network Boston, 2019
Apolipoprotein-E (ApoE) has been implicated in Alzheimer’s disease, atherosclerosis, and other unresolvable inflammatory conditions but a common mechanism of action remains elusive.
C. Yin   +28 more
semanticscholar   +1 more source

Tumor Cells Hijack Macrophage-Produced Complement C1q to Promote Tumor Growth

open access: yesCancer immunology research, 2019
The density of C1q-producing TAMs and C4d deposits, hallmarks of complement activation, are negative prognostic factors in human clear-cell renal cell carcinoma.
L. Roumenina   +32 more
semanticscholar   +1 more source

Factorization method for difference equations of hypergeometric type on nonuniform lattices [PDF]

open access: yes, 2001
We study the factorization of the hypergeometric-type difference equation of Nikiforov and Uvarov on nonuniform lattices. An explicit form of the raising and lowering operators is derived and some relevant examples are given.Comment: 21 ...
Askey R   +30 more
core   +4 more sources

The regulatory roles of C1q

open access: yesImmunobiology, 2007
C1q binds to immune complexes to elicit complement-dependent microbial killing and enhance phagocytosis. Besides this classical role, C1q also opsonizes apoptotic cells for clearance by phagocytes. C1q deficiency increases susceptibility to microbial infections and is also associated with elevated autoimmunity as characterized by increased apoptotic ...
Lu, J., Wu, X., Teh, B.K.
openaire   +2 more sources

Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium [PDF]

open access: yes, 2008
This study was prompted by the observation that decidual endothelial cells (DECs), unlike endothelial cells (ECs) of blood vessels in normal skin, kidney glomeruli and brain, express surface-bound C1q in physiologic pregnancy. This finding was unexpected,
Agostinis, C.   +9 more
core   +1 more source

Is the anti-tumor property of Trypanosoma cruzi infection mediated by its Calreticulin?

open access: yesFrontiers in Immunology, 2016
Eight to 10 million people in 21 endemic countries are infected with Trypanosoma cruzi. However, only 30% of those infected develop symptoms of Chagas’ disease, a chronic, neglected tropical disease worldwide. Similar to other pathogens, T.
Galia Andrea Ramírez-Toloza   +2 more
doaj   +1 more source

Soluble gC1qR is an autocrine signal that induces B1R expression on endothelial cells [PDF]

open access: yes, 2013
Bradykinin (BK) is one of the most potent vasodilator agonists known and belongs to the kinin family of proinflammatory peptides. BK induces its activity via two G protein-coupled receptors: BK receptor 1 (B1R) and BK receptor 2.
David, H   +10 more
core   +2 more sources

Cardiac-derived CTRP9 protects against myocardial ischemia/reperfusion injury via calreticulin-dependent inhibition of apoptosis. [PDF]

open access: yes, 2018
Cardiokines play an essential role in maintaining normal cardiac functions and responding to acute myocardial injury. Studies have demonstrated the heart itself is a significant source of C1q/TNF-related protein 9 (CTRP9). However, the biological role of
Feng, Pan   +13 more
core   +2 more sources

Anti-C1q autoantibodies, novel tests and clinical consequences

open access: yesFrontiers in Immunology, 2013
Although anti-C1q autoantibodies have been described more than four decades ago a constant stream of papers describing clinical associations or functional consequences highlights that anti-C1q antibodies are still hot and happening.
Michael eMahler   +2 more
doaj   +1 more source

Home - About - Disclaimer - Privacy