Inflammation describes a complex series of biological processes which the body initiates in response to certain stimuli that are usually, but not always, harmful to the organism. Examples of these stimuli are invading pathogens, damaged or dying cells, chemical irritants, and exposure to extreme temperatures. Inflammation is a major component of innate immunity and provides a non-specific response (as opposed to adaptive immunity). Although acute inflammation is necessary to rid the body of harmful pathogens, chronic inflammation can be destructive to healthy tissue and can both be caused by, and lead to, various diseases.

Inflammation can broadly be separated into three sequential phases.


Inflammation begins with an insult or stimulus to an organ. The source of inflammation can be a foreign body, like an invading bacteria or virus, though the source of inflammation can also be damaged cells, such as necrotic cells from a physical wound, or transformed tumor cells. The initial response may differ depending on the source of inflammation. For example, TLR2, TLR4, and TLR9 can be activated by lipoproteins on the surface of bacteria and prokaryotic DNA, causing the release of cytokines (such as IL-1β, IFNα, and IFNβ) and chemokines (such as IL-8, MCP-1 and MIP-1α) promoting immune cell activation and recruitment. It is also in this stage that the complement pathway may become activated, initiating a cascade of events ultimately resulting in C3a activation enhancing inflammation and C3b, which will lead to generation of the membrane attack complex.


At this point, C3a activation, histamine release from mast cells, and production of prostaglandin cause changes in the vasculature including vasodilation, increased blood flow, and increased vascular permeability allowing immune cells to more easily escape from blood vessels into the tissue. Immune cells, such as neutrophils and macrophages, recognize molecular patterns on the surface of invading pathogens or transformed cells and engulf these cells. The immune cells utilize cytotoxic mediators (such as reactive oxygen species) to destroy the targeted cells. Immune cells will also produce cytokines, such as TNF-α, IFN-γ, and IL-1β, which will enhance inflammation and recruit additional immune cells into the tissue.


Dead and dying cells present “find-me” and “eat-me” signals such as phosphatidylserine, oxLDL, and sphingosine-1 phosphate, which recruit scavenging phagocytes to engulf these cells and control further inflammation. Certain cells, such as macrophages, may switch to an anti-inflammatory phenotype promoting the depletion of cytotoxic mediators through arginase-1 activity. These cells also produce anti-inflammatory cytokines such as IL-10 and TGF-β. Fibroblasts activated by TNF-α and IL-1β begin tissue remodeling and repair by laying down collagen and extracellular matrix, which can produce scar tissue. Antigen presenting cells, such as dendritic cells, process antigen from the source of injury and then travel to lymph nodes where they present the antigen to naïve T cells and B cells. Naïve T cells can differentiate into helper T cells which may propagate the immune response through release of IFN-γ and IL-2. B cells differentiate into plasma B cells, which produce antibody specific to the invading pathogen, which will more readily trigger an enhanced immune response the next time it is encountered.

View our 9 step animation on Inflammation.


Inflammation can further be defined as either acute or chronic inflammation. Although acute inflammation is necessary to rid the body of foreign pathogens, inflammation that progresses to chronic inflammation can be detrimental to the organism, damaging normal tissue and may even develop into cancer.

  Acute Chronic
Sources: Harmful bacteria and viruses, necrotic cells from a physical injury Persistent exposure to particular pathogens, certain viruses, tumor cells, auto-immunity, allergic responses to benign substances
Major Cells: Primarily monocytes/macrophages and neutrophils, but also mast cells and dendritic cells Plasma B cells, helper T cells, macrophages, fibroblasts
Duration: Days Months to years
Effect: Elimination of the source of cellular injury or pathogen. Minimal damage to healthy or unrelated tissue. Consistent damage to healthy cells, development of scar tissue

Inflammation is recognized by having four cardinal symptoms (the four “-ors”): calor (heat), rubor (redness), tumor (swelling), and dolor (pain). In the 19th century, an additional symptom, loss of function, was also attributed to inflammation. Many diseases have some chronic inflammatory component, where the inflammatory stimuli is not an invading pathogen. Though there are a great number of these diseases, click on the conditions below to see how inflammation plays a role. Inflammation can also play a role in certain neurological diseases, which you can read about on our Neuroinflammation page.


Atherosclerosis begins as a build-up of cholesterol, fatty acids, and calcium in the artery which attracts macrophages in an attempt to engulf the proteins that transfer fat (such as LDL, low density lipoprotein). These macrophages turn into foam cells which accumulate and release cytokines, reactive oxygen species, and growth factors which recruit additional immune cells, including T helper 1 cells that release pro-inflammatory cytokines, amplifying the immune response at the site of the lesion.


Type 2 Diabetes

In type 2 diabetes, insulin resistance develops due to pancreatic β-cells being unable to compensate for an excess of nutrients in the blood. Stressed pancreatic cells and adipocytes can produce pro-inflammatory cytokines such as IL-1β, TNFα, and CCL2, encouraging recruitment of macrophages and lymphocytes, causing tissue inflammation. This inflammation can cause cell death or cell damage that causes further insulin resistance.


Autoimmune Diseases

Autoimmune diseases occur through an abnormal immune response against tissues or proteins that naturally occur in one’s own body. Since the elimination of the antigen or offending tissue is not possible, these diseases must typically be treated through immunosuppression. There are over 80 diseases that are characterized by autoimmunity, but here are some that you’ve probably heard of before, along with the tissue that the immune response is mounted in: psoriasis (skin), type 1 diabetes (pancreas), Crohn’s disease (digestive tract), rheumatoid arthritis (joints), lupus (connective tissue), and multiple sclerosis (central nervous system).



Inflammation can have opposing roles in cancer. During tumor initiation, type 1 inflammation can be a source of reactive oxygen species and cellular damage, causing genetic instability and may encourage the transformation of cells into a malignant phenotype. After a tumor has developed, type 2 inflammation may dominate, with cancer cells releasing immunosuppressive cytokines that down-regulate the cytotoxic response and encourage pro-resolving mediators. Cells may express immune checkpoint receptors that engage T cells to induce tolerance, allowing the tumor to escape immunosurveillance.



In allergic disease, the immune system will mount a response against harmless substances, such as pollen or certain proteins in food. This hypersensitivity to allergens causes an IgE-mediated immune response which activates mast cells to release histamine, causing a localized immune response. Though allergies are commonly treated using anti-histamines, in severe cases, it can be treated using immunosuppressive drugs such as corticosteroids.

Innate Immunity

Innate immunity is the first line of defense against invading pathogens. Its mechanisms of action are non-specific toward the invading pathogen. Some of the major features of innate immunity include: the complement cascade, phagocytosis, Toll-Like Receptors, chemotaxis, and extravasation. Skin and stomach acid serve as physical barriers to pathogens. Phagocytosis can lead to antigen presentation, which bridges innate and adaptive immunity.

Human Innate Immunity Products Mouse Innate Immunity Products
Rat Innate Immunity Products  


Inflammatory Cytokines and Chemokines, and Their Receptors

Cytokines and chemokines are small soluble proteins that cells use to communicate with one another. Cytokines can have a wide range of effects in immune cells, from inducing activation to inducing apoptosis. Chemokines are similar, but their main effect is inducing chemotaxis of cells. Both cytokines and chemokines act on specific receptors to induce their effects.

Mouse Cytokine and Chemokine Products Human Cytokine and Chemokine Products
Mouse Cytokine and Chemokine Receptor Products Human Cytokine and Chemokine Receptor Products



Neuroinflammation is a distinct type of inflammation that takes part in the central nervous system. Check out our Neuroinflammation webpage to learn more.

Cancer Inflammation

In order for a tumor to proliferate unchecked, they must develop strategies to evade detection by the immune system so that they are not targeted by apoptosis mechanisms. One method that they accomplish this is through immune checkpoint receptors that bind to ligands on immune cells which can deactivate immune cells such as lymphocytes. Check out our Immunotherapy webpage to learn more.

Major Cells of Inflammation

There are several cells involved in inflammation, and BioLegend has products that can be used in both detection and phenotyping of these cells. Click on the appropriate cell below to see a list of the products we have available for that cell type.


Human NK and NKT Cell Products Mouse NK and NKT Cell Products
Human Monocyte and Macrophage Products Mouse Monocyte and Macrophage Products
Human Neutrophil Products Mouse Neutrophil Products
Human B Cell Products Mouse B Cell Products
Human Dendritic Cell Products Mouse Dendritic Cell Products
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