An introduction to immunology and immunopathology

Open Access

Allergy, Asthma & Clinical Immunology

*Correspondence:  [e-mail] 

1

 Department of Microbiology and Immunology, Dalhousie University, 

Halifax, NS, Canada

Full list of author information is available at the end of the article

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Page 6 of 14

Marshall et al. Allergy Asthma Clin Immunol 2018, 14(Suppl 2):49

Innate immunity

Innate immunity can be viewed as comprising four 

types of defensive barriers: anatomic (skin and mucous 

membrane), physiologic (temperature, low pH and 

chemical mediators), endocytic and phagocytic, and 

inflammatory. Table 

1

 summarizes the non-specific host-

defense mechanisms for each of these barriers. Cells and 

processes that are critical for effective innate immunity 

to pathogens that evade the anatomic barriers have been 

widely studied. Innate immunity to pathogens relies 

on pattern recognition receptors (PRRs) which allow 

a limited range of immune cells to detect and respond 

rapidly to a wide range of pathogens that share common 

structures, known as pathogen associated molecular 

patterns (PAMPs). Examples of these include bacterial 

cell wall components such as lipopolysaccharides (LPS) 

and double-stranded ribonucleic acid (RNA) produced 

during viral infection.

An important function of innate immunity is the 

rapid recruitment of immune cells to sites of infection 

and inflammation through the production of cytokines 

and chemokines (small proteins involved in cell–

cell communication and recruitment). Cytokine 

production during innate immunity mobilizes many 

defense mechanisms throughout the body while also 

activating local cellular responses to infection or injury. 

Key inflammatory cytokines released during the early 

response to bacterial infection are: tumour necrosis 

factor (TNF), interleukin 1 (IL-1) and interleukin 6 

(IL-6). These cytokines are critical for initiating cell 

recruitment and the local inflammation which is 

essential for clearance of many pathogens. They also 

contribute to the development of fever. Dysregulated 

production of such inflammatory cytokines is often 

associated with inflammatory or autoimmune disease, 

making them important therapeutic targets.

The complement system is a biochemical cascade that 

functions to identify and opsonize (coat) bacteria and 

other pathogens. It renders pathogens susceptible to 

phagocytosis, a process by which immune cells engulf 

microbes and remove cell debris, and also kills some 

pathogens and infected cells directly. The phagocytic 

action of the innate immune response promotes 

clearance of dead cells or antibody complexes and 

removes foreign substances present in organs, tissues, 

blood and lymph. It can also activate the adaptive 

immune response through the mobilization and 

activation of antigen-presenting cells (APCs) (discussed 

later) [

1

, 

3

].

Numerous cells are involved in the innate immune 

response such as phagocytes (macrophages and 

neutrophils), dendritic cells, mast cells, basophils, 

eosinophils, natural killer (NK) cells and innate lymphoid 

cells. Phagocytes are sub-divided into two main cell types: 

neutrophils and macrophages. Both of these cells share 

a similar function: to engulf (phagocytose) microbes 

and kill them through multiple bactericidal pathways. 

In addition to their phagocytic properties, neutrophils 

contain granules and enzyme pathways that assist in the 

elimination of pathogenic microbes. Unlike neutrophils 

(which are short-lived cells), macrophages are long-lived