Results 11 to 20 of about 62,354 (276)

The Fc fragment of IgMs binds C1q to activate the first step of the classical complement pathway, while inhibiting complement-dependent cytotoxicity [PDF]

open access: goldThe FEBS Journal, EarlyView.
Multimeric IgM‐fragment crystallizable region (Fc) fragments retain the ability to bind C1q and initiate the classical complement pathway, leading to C4 activation and deposition in vitro. However, the Fc cores can also inhibit complement‐dependent cytotoxicity by competing with surface‐bound antibodies for C1q engagement.
Andre J. Pinto   +9 more
openalex   +2 more sources

C1q A08 Is a Half-Cryptic Epitope of Anti-C1q A08 Antibodies in Lupus Nephritis and Important for the Activation of Complement Classical Pathway

open access: yesFrontiers in Immunology, 2020
To investigate the fine epitope(s) of anti-C1q A08 antibodies and their roles in complement activation in lupus nephritis, C1q A08 and related peptides with various amino acid sequences around A08 were synthesized.
Wen-Jun Wu   +23 more
doaj   +1 more source

A non-redundant role of complement protein C1q in normal and adverse pregnancy

open access: yesExploration of Immunology, 2022
Complement component 1q (C1q) is the recognition molecule of the classical pathway of the complement system that can bind to an array of closely spaced antigen-bound immunoglobulin G (IgG) and IgM antibodies.
Chiara Agostinis   +4 more
doaj   +1 more source

AIF1+CSF1R+ MSCs, induced by TNF‐α, act to generate an inflammatory microenvironment and promote hepatocarcinogenesis

open access: yesHepatology, EarlyView., 2022
Mesenchymal stem cells subset, educated by TNF‐α, are involved to generate inflammatory microenvironment and promote hepatocarcinogenesis Abstract Background and Aims Increasing evidence suggests that mesenchymal stem cells (MSCs) home to injured local tissues and the tumor microenvironment in the liver.
Chen Zong   +9 more
wiley   +1 more source

CD93 is Selectively Expressed on Human Myeloma Cells but Not on B Lymphocytes [PDF]

open access: yesIranian Journal of Immunology, 2019
Background: CD93 has originally been known as a C1q receptor, and many studies have demonstrated that CD93 is expressed on hematopoietic stem cells, B cell progenitors, myeloid and monocytic cells.
Shohreh Fakhari   +4 more
doaj   +1 more source

Complement, C1q, and C1q-Related Molecules Regulate Macrophage Polarization [PDF]

open access: yesFrontiers in Immunology, 2014
Complement is a critical system of enzymes, regulatory proteins, and receptors that regulates both innate and adaptive immune responses. Natural mutations in complement molecules highlight their requirement in regulation of a variety of human conditions including infectious disease and autoimmunity.
Bohlson, Suzanne S.   +4 more
openaire   +3 more sources

C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation [PDF]

open access: yes, 2015
Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation.
Agostinis, C   +9 more
core   +3 more sources

Peptide inhibitor of complement C1 (PIC1), a novel suppressor of classical pathway activation: mechanistic studies and clinical potential

open access: yesFrontiers in Immunology, 2014
The classical pathway of complement plays multiple physiological roles including modulating immunological effectors initiated by adaptive immune responses as well as an essential homeostatic role in the clearance of damaged self-antigens.
Julia A Sharp   +5 more
doaj   +1 more source

A common theme in interaction of bacterial immunoglobulin-binding proteins with immunoglobulins illustrated in the equine system [PDF]

open access: yes, 2008
The M protein of Streptococcus equi subsp. equi known as fibrinogen-binding protein (FgBP) is a cell wall-associated protein with antiphagocytic activity that binds IgG. Recombinant versions of the seven equine IgG subclasses were used to investigate the
Abi-Rached   +49 more
core   +4 more sources

SLE: Novel Postulates for Therapeutic Options

open access: yesFrontiers in Immunology, 2020
Genetic deficiency in C1q is a strong susceptibility factor for systemic lupus erythematosus (SLE). There are two major hypotheses that potentially explain the role of C1q in SLE.
Kinga K. Hosszu   +3 more
doaj   +1 more source

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