Chemokine that acts primarily on neutrophils;
CXC chemokines
have one amino acid residue separating the first two of the four conserved cysteine residues
CXC chemokines
have the first two conserved cysteine residues adjacent
C-C chemokines
generally attract monocytes, eosinophils, basophils, and lymphocytes, but are less potent chemoattractants for neutrophils
CC Chemokines
lack the first and third of the four conserved cysteines. These chemokines e.g., (lymphotactin, XCL1) are relatively specific for lymphocyte
C Chemokines
contain three amino acids between the two cysteines; This chemokine exists in two forms: a cell surface–bound protein induced on endothelial cells by inflammatory cytokines & a soluble form derived by proteolysis of the membrane-bound protein
CX3C Chemokines
CX3CL1 is also known as
fractalkine
collection of plasma proteins that function mainly in host defense against
microbes and in pathologic inflammatory reactions
Complement System
cause increased vascular permeability, chemotaxis, and opsonization
Complement System
The critical step in complement activation is
Proteolysis of the third component or C3
triggered by binding of C1 to antibody (IgM or IgG) that has combined with antigen
Classical Pathway
triggered by microbial surface molecules (e.g., endotoxin, or lipopolysaccharide [LPS]), complex polysaccharides, cobra venom, and other substances, in the absence of antibody.
Alternative Pathway
plasma mannose-binding lectin binds to carbohydrates on microbes and directly activates C1
Lectin Pathway
C5a, C3a, and, to a lesser extent, C4a are called
Anaphylatoxins
activates the lipoxygenase pathway of AA metabolism in neutrophils and monocytes; also a chemotactic agent for neutrophils
C5a
C3b and its cleavage product inactive C3b (iC3b)
Opsonization and Phagocytosis
membrane attack complex on cells makes these cells permeable to water and ions and results in osmotic lysis of the cell
Cell lysis
This role of complement is particularly important for killing microbes such as:
Neisseria
blocks the activation of C1, the first protein of the classical complement pathway.
C1 inhibitor
are two proteins that are linked to plasma membranes by a glycophosphatidylinositol (GPI) anchor
DAF (Decay Accelerating Factor) & CD59