No prior contact with microorganisms or immunization

Roles: 1. To clean up debris from dying cells andrepairing damage tissues 2. To kill invading microbes 3. To activate adaptive immune response

Specificity: 1. Non-specific : Indicate a degree of resistance to infections in general 2. Specific: Resistance to a particular pathogen is concerned

Barrier

No lag phase present, rapid immune response

short duration effectiveness

Limited diversity hence limited specificity

Mmemory cells are absent

Reaction against foreign bodies

When the skin is cut, bacteria and other pathogens enter wound

The tissue damage and presence of bacteria to local mast cells trigger a release of histamine granules to surrounding tissues

Histamine granules increase permeability to local blood vessels and stimulate influx of other immune cells (chemotaxis)

Since local blood vessels are dilated, plasma flow to area is increased causing redness, swelling and pain

Neutrophils enter the infected tissue from local blood vessels and engulf bacteria and damaged cells (phagocytosis)

Macrophages secrete cytokines that attract immune cells to the site of wound and activate tissue repair

Inflammatory response continues until the foreign material is eliminated and the wound is repaired

Cell lysis and viral neutralization: The MAC complex creates a pore in the cell membrane, disrupting cell homeostasis and causing cellular lysis.

Chemotaxis: C5a is an important chemoattractant for neutrophils, eosinophils, basophils, and monocytes. The development of a C5a gradient at sites of complement activation assists in the recruitment of leukocytes to the area of antigenic challenge.

Clearance of immune complexes: The removal of antigen-antibody complexes from the circulation depends upon C3b. Via C3b, antigen-antibody complexes bind to complement receptors on circulating red blood cells. As the RBCs pass through the spleen and liver, the coated complexes are stripped off of the RBCs by resident phagocytes.

Opsonization: When an antigenic particle is coated with C3b, it assists in the adherence and ultimate ingestion of the particle by the phagocytic cell that has a receptor for C3b. The C5a fragment also enhances phagocytosis by stimulating phagocytic cells to ingest C3b-coated antigens.

Anaphylatoxin/vascular changes: The fragments C3a, C4a, and C5a are capable of binding to specific receptors on mast cells and basophils, triggering granule release by these cells. The release of histamine leads to vascular changes, including increased vascular permeability.

Monocyte - Increases phagocytic ability

Macrophage - Phagocytosed bacteria by releasing microbicidal molecule

Dendritic cells - Take up Ag by phagocytosis,receptor mediated endocytosis and micropinocytosis

Neutrophils - Involves in phagocytosis (Very important at “clearing” bacterial infection and inflammation)

Eosinophils- Kills Ab-coated parasites through degranulation

Basophils - They are thought to mediate immediate (type I hypersensitivity reactions such as asthma and anaphylaxis

Mast cell - Activated mast cells releases leukotrienes which attract eosinophils to site of worm infection & discharge granule content

Natural killer cells - recognize and kill some abnormal cells with low MHC Class I

Cytokines