They are the major players in acute inflammation, and their main function is phagocytosis of microbe and subsequent killing of the microbe by an oxidative “burst” leading to release of reactive oxygen species as well as release of neutrophil granule content containing acidic and alkaline phosphatases, defensins, and peroxidase.

Macrophages are another group of phagocytic cells which are larger than neutrophils and are predominantly involved in chronic inflammation. In addition to their phagocytic and microbicidal activity, they also bridge the innate immune response to the adaptive immune response by presenting the antigen to T lymphocytes.

Like macrophages, dendritic cells also present the antigen to the T-helper cell. They are also called professional antigen-presenting cells (APCs). Naïve or immature DCs can take up the antigen but are poor APCs [5]. On activation by TLR signaling they become mature DCs and acquire co-stimulatory molecules, and thus become efficient at processing the antigen and presenting it to CD4 cells. In addition they secrete chemokine (C-C motif) ligand 18 (CCL18) that attracts naive T cells toward the dendritic cell in the lymph nodes thus increasing the interaction between DCs and T cells.

They comprise about 5–10 % of circulating lymphocytes and as the name suggests, they have an inherent property to kill the target cell. The usual targets are virus-infected cells or tumor cells. NK cells have killer activation receptors and killer inhibition receptors on their cell surface in addition to receptor for immunoglobulin type G [6]. The inhibiting receptors interact with MHC class I molecules on cells and thus prevent killing of normal cells. A cell such as a tumor or virus-infected cell that lacks MHC class I will be recognized by NK cells and be killed by induction of apoptosis or by release of perforins and granzyme from its granules. NK cells also secrete IFN-γ and thus augment the CD8 T-cell response against virally infected cells. In addition, NK cells can also kill cells coated by antibodies by binding to them via IgG receptors by a mechanism termed antibody-dependent cellular cytotoxicity (ADCC).

The complement system primarily helps to fight bacterial infections by generating multiple complement products during its activation. Complement system can be activated by immune complexes, bacterial products, or mannose binding lectins [7]. Early complement products like C4b and C2a act as opsonins and help in the phagocytosis of bacteria by neutrophils and macrophages. C3a and C5a act as chemo-attractants and help in recruiting neutrophils to the site of inflammation and as anaphylatoxins help in release of histamine from basophils and mast cells. The complex formed at the end by late complement components causes lysis of the bacterial cell.

T cells can be broadly divided into CD4 or T-helper (Th) and CD8 or T cytotoxic cells (Tc). CD4 Th cells are divided into many different subsets based on the cytokine produced, transcription factor needed for their development, and chemokine receptors expressed by them (Fig. 2.1) [8]. Depending on the kind of pathogen or inciting stimuli, different subsets of Th cells are generated.