Processes involved in the activation of any of the steps of the complement cascade, which allows for the direct killing of microbes, the disposal of immune complexes, and the regulation of other immune processes; the initial steps of complement activation involve one of three pathways, the classical pathway, the alternative pathway, and the lectin pathway, all of which lead to the terminal complement pathway.

Processes involved in the activation of any of the steps of the alternative pathway of the complement cascade which allows for the direct killing of microbes and the regulation of other immune processes.

Processes involved in the activation of any of the steps of the classical pathway of the complement cascade which allows for the direct killing of microbes, the disposal of immune complexes, and the regulation of other immune processes.

Interacting selectively with an insulin-like growth factor, any member of a group of polypeptides that are structurally homologous to insulin and share many of its biological activities, but are immunologically distinct from it.

An immune response mediated through a body fluid.

Interacting selectively with profilin, an actin-binding protein that forms a complex with G-actin and prevents it from polymerizing to form F-actin.

Interacting selectively with tropomyosin, a protein associated with actin filaments both in cytoplasm and, in association with troponin, in the thin filament of striated muscle.

Interacting selectively with ATP, adenosine 5'-triphosphate, a universally important coenzyme and enzyme regulator.

Interacting selectively with GTP, guanosine triphosphate.

Interacting selectively with a macrolide, any of a large group of structurally related antibiotics produced by Streptomyces species.

Interacting selectively with the immunosuppressant FK506.

Interacting selectively with any mono-, di- or trisaccharide carbohydrate.

The regrowth of muscle tissue to repair injured or damaged muscle fibers in the postnatal stage.

The series of molecular signals generated by the accumulation of normal or misfolded proteins in the endoplasmic reticulum and leading to activation of transcription by NF-kappaB.