Eicosanoids include prostaglandins that produce fever and the dilation of blood vessels and leukotrienes that attract certain white blood cells (leukocytes). Growth factors and cytotoxic factors also regulate inflammatory response. These cytokines and other chemicals recruit immune cells to the site of infection and promote healing of damaged tissue following the removal of pathogens. NFkB plays a key role in regulating the immune response to infection. JAK/STAT pathway is also important.

The immune system protects organisms from infection with layered defenses of increasing specificity. The innate immune system provides an immediate, but non-specific response. It has no immunological memory and is found in nearly all forms of life. Phagocytosis is an important feature of cellular innate immunity, which is performed by macrophages, neutrophils, and dendritic cells that engulf pathogens or particles.

Toll-like receptors (TLRs) are receptors that play key roles in the innate immune system. TLRs are a type of pattern recognition receptors (PRRs) and recognize molecules that are broadly shared by pathogens but distinguishable from host molecules. These molecules are collectively referred to as pathogen-associated molecular patterns (PAMPs). TLRs together with the interleukin-1 (IL-1) receptors form a receptor superfamily, which is known as the "Interleukin-1 Receptor / Toll-Like Receptor Superfamily". All members of this family have a so-called TIR (Toll-IL-1 receptor) domain. Thirteen TLRs (TLR1 to TLR13) have been identified in humans and mice altogether. In humans, TLR1, 2, 4, 5, and 6 are cell membrane associated and respond primarily to bacterial surface-associated PAMPs. The second group, TLR3, 7, 8, and 9 are expressed on the surface of endosomes, where they respond primarily to nucleic acid based PAMPs from viruses and bacteria. Upon ligand binding, TLRs activate two major signaling pathways: the NFkB and the MAPK (p38 and JNK) pathways.

In jawed vertebrates, the immune system can adapt its response during an infection to improve the recognition of pathogens. This improved response is called adaptive immunity, which is retained even after pathogens have been eliminated. This kind of immunological memory allows the immune system to mount faster and stronger responses every time a particular pathogen is encountered again.

T cells and B cells play important roles in adaptive immune response. White blood cells are comprised of neutrophils, eosinophils, basophils, lymphocytes (T-cell, B-cell, and natural killer cell), monocytes, macrophages and dendritic cells. Dendritic cells are antigen presenting cells (APC) that activate T-lymphocytes. Both B-cells and T-cells carry receptor molecules that recognize specific targets. B-cells are involved in the humoral immune response (HIR - the aspect of immunity that is mediated by secreted antibodies), whereas T-cells are involved in cell-mediated immune response. The B-cell antigen (small fragment of the pathogen) - specific receptor is an antibody molecule on the B-cell surface that recognizes whole pathogens without any need for antigen processing. Each lineage of B-cells expresses a different antibody, so the complete set of B-cell antigen receptors represents all the antibodies that the body can manufacture. In contrast, T-cells recognize a "non-self" target, such as a pathogen, only after antigens have been processed and presented in combination with a "self" receptor called a major histocompatibility complex (MHC) molecule. There are two major subtypes of T-cells: the killer T-cells and the helper T-cells. The killer T-cells only recognize antigens coupled to Class I MHC molecules while the helper T-cells only recognize antigens coupled to Class II MHC molecules. The killer T-cells are activated when their T-cell receptors (TCR) bind to specific antigens complexed with the MHC Class I receptors of another cell. Recognition of this MHC-antigen complex is aided by a co-receptor on the T-cell, called CD8. The T-cell then travels throughout the body in search of cells where the MHC I receptors bear this antigen. The helper T-cells regulate both the innate and adaptive immune responses and help determine which types of immune responses the body will initiate to respond to a particular pathogen. These helper T-cells have no cytotoxic activity and do not kill infected cells or clear pathogens directly, they instead control the immune response by directing other cells (B-cells, macrophages and killer T-cells) to perform these tasks. The MHC-antigen complex is recognized by the helper T-cell's CD4 co-receptor. Depending on the size, cytokine signals received, these cells differentiate into Th1, Th2, Th3, Th17, or other subsets, which secrete different cytokines.

Regulatory T-cells (Treg-cells) are crucial for the maintenance of immunological tolerance. Their major role is to shut down T-cell mediated immunity toward the end of an immune reaction and to suppress auto-reactive T-cells that have escaped the process of negative selection in the thymus since the thymus is the principal organ responsible for the T-cell maturation. Two major classes of CD4+ regulatory T-cells have been described, including the naturally occurring Treg-cells and the adaptive Treg-cells. Naturally occurring Treg-cells (also known as CD4+CD25+FoxP3+ Treg-cells) arise in the thymus, whereas the adaptive Treg-cells (also known as Tr1 cells or Th3 cells) originate during a normal immune response. Naturally occurring Treg-cells can be distinguished from other T cells by the presence of an intracellular molecule called FoxP3.

The immune system is a remarkably effective structure with specificity, inducibility, and adaptation. Deregulation of an immune system falls into three broad categories: immunodeficiency, autoimmunity, and hypersensitivity.

Immunodeficiency occurs when one or more of the components of the immune system are inactive. Obesity, alcoholism, and drug abuse are common causes of poor immune function. Acquired immunodeficiency largely contributes to AIDS (Acquired Immune Deficiency Syndrome), which is caused by the Human Immunodeficiency Virus (HIV).

Overactive immune response is the other end of immune dysfunction. Hypersensitivity is a form of an overactive immune response. Allergies are the most common type of hypersensitivity. Symptoms can range from mild discomfort to death. Anti-inflammatory drugs are often used to control the symptoms. Glucocorticoids are the most powerful of these drugs. When the immune system fails to properly distinguish between self-antigens and non-self antigens and attacks part of the body, autoimmunity occurs. Autoimmune diseases include Crohn's disease, diabetes mellitus type 1, lupus, psoriasis, and rheumatoid arthritis.

T-Cell & B-Cell Activation, T-Cell Anergy and Immune Tolerance, Th1-Th2-Th3, or Th17 for Autoimmunity and Inflammation PCR arrays can be used to investigate gene expression changes associated with inflammatory response. To profile the expressions of various cytokines, one can use SABiosciences' Inflammatory Cytokines and Receptors, Common Cytokines, Chemokines and Receptors, Interferon Alpha, Beta Response, and Interferons and Receptors PCR arrays. NFkB or JAK/STAT PCR arrays can also be used to study the respective signaling pathways.