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Human Skin Mast Cells Express Complement Factors C3 and C5
TLDR
Human mast cells can produce and secrete C3, whereas β-tryptase can act on C3 to generate C3a and C3b, raising the likelihood that mast cells engage complement to modulate immunity and inflammation in vivo.
Anaphylatoxin binding and degradation by rat peritoneal mast cells. Mechanisms of degranulation and control.
TLDR
It is proposed that the cationic C3a molecule activates rat mast cells in a secretory and nonlytic manner by a nonspecific mechanism similar to that of other polybasic compounds.
Generation of anaphylatoxins by human beta-tryptase from C3, C4, and C5.
TLDR
Results suggest beta-tryptase might generate complement anaphylatoxins in vivo at sites of inflammation, such as the airway of active asthma patients where the pH is acidic and where elevated levels of beta- tryptase and complementAnaphyl atoxins are detected.
Tissue distribution of products of the mouse decay‐accelerating factor (DAF) genes. Exploitation of a Daf1 knock‐out mouse and site‐specific monoclonal antibodies
TLDR
A Daf1 gene knock‐out mouse arising as the first product of a strategy for targeting one or both Daf genes is described and the sensitive tyramide fluorescence method is utilized to enhance the immunohistochemical detection of murine DAF protein.
Differential cytokine expression of human retinal pigment epithelial cells in response to stimulation by C5a
TLDR
C5a stimulation of RPE cells may play a role in regulating leucocyte function during ocular inflammation in which there is complement activation, and induces increased expression of IL‐1β, IL‐6, MCP‐1 and GM‐CSF mRNAs as well as IL‐8 mRNA.
Cloning and characterization of the guinea pig C5a anaphylatoxin receptor: interspecies diversity among the C5a receptors.
TLDR
The guinea pig system is perhaps unique for exhibiting cross-reactivity with human complement components and its high sensitivity to anaphylatoxins, therefore residues critical for C5a binding have been conserved between these species.
Molecular cloning of two isoforms of the guinea pig C3a anaphylatoxin receptor: alternative splicing in the large extracellular loop.
TLDR
Evidence indicates that alternative splicing occurred in the large EC loop that accounts for these two isoforms of guinea pig C3aR, which is a potent spasmogen and recently been described as an eosinophil and mast cell chemotactic factor that mediates a number of inflammatory reactions.
Demonstration of a specific C3a receptor on guinea pig platelets.
TLDR
It is concluded that guinea pig platelets have specific surface receptors to C3a and that human platelets appear devoid of receptors to the anaphylatoxin.
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