Innate Immune System

Pathogens have pathogen associated molecular patterns (PAMPs) expressed on their cell surface, so when they enter the body, sentinel cells (which express pattern recognition receptors (PRRs)) can bind to them.

Following this binding, there can be a number of responses:

1.    Cell recruitment (and inflammation)

·         Mast cells release histamine in very high concentrations within the tissues, as well as cytokines and chemokines

·         The venule becomes inflamed, causing a dilation of blood vessels and slowing down blood flow. Tight junctions also break down causing leakiness in the vasculature

·         This results in the attraction of immune effector cells from the blood

2.    Phagocytosis

·         Phagocytes: neutrophils, monocytes, macrophages, mast cells and dendritic cells

·         Opsonins (any substance that enhances phagocytosis by tightly binding the microbe to the phagocyte) can coat the antigens, allowing for phagocytosis to occur

3.    Activation of the complement cascade:

The complement cascade can be activated in 3 different ways:

                       I.        Classical pathway

Ø  Antibodies bind to the antigens of pathogens in the bloodstream, forming an antigen/antibody complex

Ø  This then activates C1 (irrelevant)

                     II.        Lectin pathway

Ø  Mannose binding lectin (MBL) and C-reactive protein (CRP) are acute phase proteins

Ø  They bind directly to the pathogen and activate the complement cascade

                    III.        Alternative pathway

Ø  There is spontaneous C3 hydrolysis, causing the release of C3a (chemoattractant) and C3b which binds to the pathogen

Once activation occurs:

C3

• ·         When complement protein C3 gets activated, the active enzyme C3b is released and a…