Educational Notes

Basic Concepts in Immunology and Components of the Immune System

Abouelhag H. A. *

Microbiology and Immunology Dept., National Research Centre, Dokki, Giza, Egypt, 12622.

Received: 08-04-2026 Accepted: 22-04-2026 Published online: 28-04-2026

DOI: https://doi.org/10.33687/ricosbiol.04.04.120

Based on the handout: Abouelhag, H. (2010). Basic immunology, MLT 360: Hand out 2010/2011 [Unpublished course handout].

Supplementary references: Abbas et al., 2022; Murphy, Weaver, & Berg, 2022; Punt et al., 2023; Delves et al., 2023; Huang et al., 2023; Shafqat et al., 2023; Wang et al., 2024; Nature Portfolio, 2024; Science Immunology, 2025.

Abstract

This chapter introduces the fundamental concepts of immunology, focusing on the relationship between infection and the host immune system. It defines key terms such as infection, pathogenicity, and normal microbiota, and classifies infections by localisation, incidence, etiology, and systematic site. The chapter then distinguishes between the two major branches of the immune system: nonspecific (innate) immunity and specific (adaptive) immunity. The cellular components—including lymphocytes (B cells, T cells, natural killer cells), mononuclear phagocytes, granulocytes, mast cells, and dendritic cells—are described in terms of their origin, maturation, and function. The primary lymphoid organs (bone marrow and thymus) and secondary lymphoid tissues (spleen, lymph nodes, and mucosa‑associated lymphoid tissue) are explained as sites of lymphocyte development and antigen encounter. Finally, the physical and mechanical barriers that constitute the first line of defence—skin, mucous membranes, and associated secretions—are reviewed, with special attention to the role of M cells in mucosal immunity. Together, these elements provide the foundation for understanding how the body recognises and defends against microbial invaders while maintaining self‑tolerance.

Keywords:

Infection, pathogenicity, normal microbiota, innate immunity, adaptive immunity, B lymphocytes, T lymphocytes, natural killer cells, macrophages, neutrophils, dendritic cells, thymus, bone marrow, spleen, lymph nodes, mucosal‑associated lymphoid tissue (MALT), M cells, skin barrier, lysozyme, lactoferrin, first line of defence.

Learning Objectives

After studying this chapter, you should be able to:

1. Define infection, pathogenicity, and the normal microbiota.

2. Distinguish between nonspecific (innate) and specific (adaptive) immunity.

3. List the major cells of the immune system and describe their primary functions.

4. Identify the primary and secondary lymphoid organs and explain their roles.

5. Explain how physical and mechanical barriers contribute to first‑line defense, including the role of M cells.

1. Infection and Disease

1.1 Definitions

· Infection – an interaction between a host and a microorganism that involves tissue damage (Abouelhag, 2010, p. 4).

· Pathogenicity – the ability of a microorganism to produce pathologic changes or disease.

· Normal microbiota (normal flora) – the mixture of microorganisms regularly found on skin and mucous membranes; they help prevent colonisation by pathogens (Wang et al., 2024).

1.2 Classification of Infection (Detailed Explanation)

Infections can be classified according to several criteria, each providing clinically useful information about the behaviour, spread, and impact of the infectious agent (Abouelhag, 2010, p. 4). The table below summarises the classification, followed by a detailed explanation of each category.

Basis	Types
Localisation	Local, general (systemic), latent
Incidence	Sporadic, enzootic, epizootic
Etiology	Primary, secondary, mixed
Systematic (site)	Respiratory, urinary tract, etc.

A. Classification by Localisation (Site of Infection within the Body)

This refers to the anatomical distribution of the infection.

· Local infection – The microorganism remains confined to a single, well‑defined area of the body. Examples include a boil (furuncle) on the skin or a localised abscess. The host’s inflammatory response typically walls off the infection, preventing systemic spread (Murphy et al., 2022).

· General (systemic) infection – The microorganism spreads throughout the body via the bloodstream or lymphatic system. Bacteraemia (bacteria in blood) or septicaemia (systemic illness with fever, tachycardia, and petechial haemorrhages) are examples (Abouelhag, 2010, p. 5). Systemic infections often produce generalised signs such as fever, malaise, and lymphadenopathy.

· Latent infection – The microorganism remains dormant within the host for a prolonged period without producing detectable signs of disease. However, the immune system may still produce antibodies that can be detected by serological tests (Abouelhag, 2010, p. 4). Examples include herpesviruses (e.g., varicella‑zoster virus) and Mycobacterium tuberculosis. Reactivation can occur when host immunity is compromised (Punt et al., 2023).

B. Classification by Incidence (Frequency and Pattern in a Population)

This classification describes how often and in what pattern an infection occurs within a host population.

· Sporadic infection – Isolated cases occur irregularly and unpredictably, with no clear pattern. For example, a single case of tetanus in a community is considered sporadic (Abouelhag, 2010, p. 4).

· Enzootic infection – A disease that recurs regularly (endemic) in a particular animal host population within a defined geographic area. For example, Lyme disease is enzootic in certain rodent and tick populations. The term is analogous to “endemic” in human epidemiology (Abbas et al., 2022).

· Epizootic infection – A disease suddenly affects a large number of animals in a population over a short period, then rapidly declines. This is analogous to an “epidemic” in humans. Examples include avian influenza outbreaks in poultry (Abouelhag, 2010, p. 4; Delves et al., 2023).

C. Classification by Etiology (Cause or Sequence of Infection)

This classification is based on the cause or the order in which different microorganisms contribute to disease.

· Primary infection – Caused by a single species of microorganism that initiates the disease process. For example, infection with Mycobacterium tuberculosis causing primary tuberculosis (Abouelhag, 2010, p. 4).

· Secondary infection – Occurs when a primary infection weakens the host’s defences, allowing a different microorganism to cause an additional infection. For example, viral influenza (primary) may be followed by bacterial pneumonia caused by Streptococcus pneumoniae or Staphylococcus aureus (Abouelhag, 2010, p. 4).

· Mixed infection – Caused by more than one microorganism simultaneously, making diagnosis and treatment more difficult. For example, certain types of pneumonia may involve both bacteria and viruses, or a wound infection may contain multiple bacterial species (Abouelhag, 2010, p. 4; Wang et al., 2024).

D. Classification by Systematic Site (Anatomical System Affected)

This classification is based on the organ system involved. It is the most common clinical classification and guides both diagnosis and treatment.

· Respiratory tract infections – Examples: common cold (rhinovirus), influenza, pneumonia, tuberculosis.

· Urinary tract infections – Examples: cystitis, pyelonephritis, often caused by Escherichia coli.

· Gastrointestinal infections – Examples: gastroenteritis (rotavirus, Salmonella), hepatitis.

· Nervous system infections – Examples: meningitis, encephalitis.

· Skin and soft tissue infections – Examples: cellulitis, impetigo, abscesses.

· Cardiovascular infections – Examples: endocarditis, sepsis.

(Murphy et al., 2022)

1.3 Transmission

· Direct – immediate contact, exhaled droplets, scales, discharge.

· Indirect – insects carry microorganisms mechanically.

1.4 Why Some Infections Spread More Easily

Factors that increase infectivity include airborne survival of the agent, susceptibility of body surfaces (e.g., respiratory tract > intact skin), large number and frequent release of microorganisms, and strain‑specific communicability.

1.5 Host and Environmental Factors

· Immune status, age.

· Gender.

· General health.

· Population density.

· Sanitation level.

1.6 Special Terms

· Bacteraemia – microorganisms in blood/lymph.

· Septicemia – infection with systemic symptoms (fever, tachycardia, petechial haemorrhages).

· Toxaemia – toxins in the blood (e.g., tetanus).

· Pyaemia – pus circulating with multiple abscesses.

2. The Immune System: Overview

· Immunity (Latin immunis – free of burden) – the general ability to resist infection or disease.

· Immunology – the science that studies immune responses, including self/nonself discrimination (Science Immunology, 2025).

2.1 Two Types of Immune Responses

Feature	Nonspecific (Innate / Natural) Immunity	Specific (Adaptive) Immunity
Specificity	Broad (recognises general patterns)	Highly specific (recognises individual antigens)
Memory	None (same response each time)	Yes (improves on repeated exposure)
Response time	Immediate (minutes to hours)	Slower (days for primary response)
Main components	Physical barriers, phagocytes, complement, NK cells	B cells, T cells, antibodies

Both systems work together to eliminate pathogens (Murphy et al., 2022).

3. Cells of the Immune System

All leukocytes originate from pluripotent haematopoietic stem cells in fetal liver and bone marrow.

3.1 Lymphoid Cells (Major cells of specific immunity)

Cell Type	Maturation Site	Main Function
B cells	Bone marrow	Produce antibodies (plasma cells); present antigens
T cells	Thymus	Helper T cells (CD4+), cytotoxic T cells (CD8+), regulatory T cells
Natural Killer (NK) cells	Bone marrow	Kill virus‑infected cells and tumour cells

(Abbas et al., 2022)

3.2 Mononuclear Phagocytes

· Monocytes – circulate in blood, then migrate into tissues and mature into macrophages.

· Macrophages – highly phagocytic; act as antigen‑presenting cells (APCs); have receptors for antibodies and complement (opsonisation).

3.3 Granulocytes (Polymorphonuclear Leukocytes – PMNs)

Type	Function
Neutrophils	Most abundant; primary phagocyte in acute inflammation; kill via lytic enzymes and reactive oxygen intermediates (Shafqat et al., 2023).
Eosinophils	Defend against parasites (helminths, protozoa); release cationic proteins.
Basophils	Non‑phagocytic; release histamine and other mediators; involved in allergies (bind IgE).

3.4 Other Important Cells

· Mast cells – connective tissue; contain histamine granules; key in inflammation and hypersensitivity.

· Dendritic cells – most potent APCs; link innate and adaptive immunity by presenting antigens to T cells (Huang et al., 2023; Nature Portfolio, 2024).

4. Organs and Tissues of the Immune System

4.1 Primary Lymphoid Organs (where lymphocytes mature)

Organ/Tissue	Function
Bone marrow	Site of B‑cell maturation; origin of all immune cells.
Thymus	Site of T‑cell maturation (positive and negative selection).

(Delves et al., 2023)

4.2 Secondary Lymphoid Organs/Tissues (where antigen encounter occurs)

Organ/Tissue	Function
Spleen	Filters blood; traps blood‑borne antigens.
Lymph nodes	Filter lymph; traps antigens from tissues.
Mucosa‑associated lymphoid tissue (MALT)	Includes GALT (gut), BALT (bronchial), SALT (skin).

5. Physical and Mechanical Barriers (First Line of Defense)

5.1 Skin

· Thick outer layer of keratin (microbes cannot digest).

· Continuous shedding of epithelial cells.

· Dryness and mild acidity (pH 5–6) inhibit microbial growth.

· Sebum forms a protective film.

· Normal skin microbiota competes with pathogens.

· Skin‑associated lymphoid tissue (SALT) – contains Langerhans cells (dendritic cells) and intraepidermal lymphocytes (T cells).

(Murphy et al., 2022)

5.2 Mucous Membranes

Mucous membranes line the respiratory, digestive, and urogenital tracts. Mucus traps microorganisms, and secretions contain lysozyme (breaks bacterial cell walls), lactoferrin (binds iron), and lactoperoxidase (produces superoxide radicals). In addition to these chemical defences, the mucosal surface possesses specialised cells and lymphoid tissues that form an integrated immune barrier.

M Cells: Specialised Antigen‑Sampling Cells

A key component of mucosal immunity is the M cell (microfold cell) . M cells are specialised epithelial cells found primarily in the follicle‑associated epithelium of the gut‑associated lymphoid tissue (GALT) , including Peyer’s patches in the small intestine, as well as in the tonsils, adenoids, and bronchial‑associated lymphoid tissue (BALT) (Murphy et al., 2022).

Unique structural features:

Unlike adjacent columnar epithelial cells, M cells lack a brush border (microvilli) on their apical surface. Instead, they have irregular microfolds that facilitate the adherence and uptake of luminal antigens. On their basolateral side, M cells possess a deep intraepithelial pocket that contains a dense cluster of lymphocytes (B cells, T cells) and macrophages (Punt et al., 2023).

Mechanism of antigen sampling:

M cells do not digest antigens for presentation. Instead, they act as gatekeepers that transport intact antigens (microbes, particles, soluble macromolecules) from the gut lumen to the underlying immune cells. The process involves:

1. Adherence – pathogens or particles bind to specific receptors (e.g., glycoprotein 2, integrins) on the M cell surface.

2. Transcytosis – the antigen is internalised and transported across the cell in endocytic vesicles.

3. Release – the antigen is discharged into the intraepithelial pocket, where it is immediately captured by resident dendritic cells or macrophages (Abbas et al., 2022; Nature Portfolio, 2024).

Immune consequences:

Once the antigen is delivered, dendritic cells (and some macrophages) process it and migrate to the lymphoid follicles. There, they present the antigen to naive B and T cells, initiating an adaptive immune response. B cells differentiate into IgA‑secreting plasma cells, and the resulting secretory IgA (sIgA) is transported back across the epithelium into the lumen, where it neutralises pathogens and prevents their attachment (Wang et al., 2024; Delves et al., 2023).

Clinical relevance:

Some pathogens have evolved to exploit M cells as portals of entry. For example, Salmonella typhi, Shigella flexneri, and prions use M cell transcytosis to invade the host. Conversely, oral vaccines are designed to target M cells to induce effective mucosal immunity (Punt et al., 2023).

Mucosa‑Associated Lymphoid Tissue (MALT)

The collection of M cells, underlying lymphoid follicles, and diffuse immune cells constitutes the mucosa‑associated lymphoid tissue (MALT) . MALT can operate by two basic mechanisms:

· Antigen sampling via M cells leads to activation of B and T cells in organised lymphoid follicles.

· Direct antigen contact with dendritic cells that extend processes between epithelial cells can also occur.

Plasma cells derived from MALT follicles secrete secretory IgA (sIgA) , which is then transported into the lumen to neutralise specific antigens. (Wang et al., 2024)

5.3 Other Systems

· Respiratory – mucociliary blanket, alveolar macrophages, coughing/sneezing.

· Gastrointestinal – gastric acid (pH 2‑3), pancreatic enzymes, bile, peristalsis, normal gut microbiota.

· Genitourinary – urine flushing, acidic vaginal environment (lactic acid from Lactobacillus).

· Eye – tears contain lysozyme, lactoferrin, and sIgA.

Summary

· The immune system comprises innate (nonspecific) and adaptive (specific) branches that cooperate to defend the host (Murphy et al., 2022).

· Key cellular players include B cells, T cells, NK cells, macrophages, neutrophils, and dendritic cells (Abbas et al., 2022; Punt et al., 2023).

· Primary lymphoid organs (bone marrow, thymus) produce and mature lymphocytes; secondary organs (spleen, lymph nodes, MALT) are sites of antigen encounter and response initiation (Delves et al., 2023).

· Physical and mechanical barriers (skin, mucous membranes, secretions) form the first line of defence. Within mucous membranes, M cells play a critical role in sampling luminal antigens and initiating mucosal immune responses.

Review Questions

1. What is the difference between an infection and a disease?

2. Compare and contrast innate immunity with adaptive immunity.

3. List four types of granulocytes and their primary functions.

4. Why is the thymus considered a primary lymphoid organ?

5. Name three antimicrobial substances found in tears and mucus.

6. Describe the structure and function of M cells in mucosal immunity.

References

Abouelhag, H. (2010). Basic immunology, MLT 360: Hand out 2010/2011 [Unpublished course handout].

Abbas, A. K., Lichtman, A. H., & Pillai, S. (2022). Cellular and molecular immunology (10th ed.). Elsevier.

Delves, P. J., Martin, S. J., Burton, D. R., & Roitt, I. M. (2023). Roitt's essential immunology (14th ed.). Wiley‑Blackwell.

Huang, Q., et al. (2023). Deciphering tumor‑infiltrating dendritic cells in the single‑cell era. Experimental Hematology & Oncology, 12(1), 45. https://doi.org/10.1186/s40164-023-00459-2

Murphy, K., Weaver, C., & Berg, L. (2022). Janeway's immunobiology (10th ed.). W.W. Norton & Company.

Nature Portfolio. (2024). Innate immunity. Nature. https://www.nature.com/subjects/innate-immunity

Punt, J., Stranford, S. A., Jones, P. P., & Owen, J. A. (2023). Kuby immunology (8th ed.). Macmillan Education.

Science Immunology. (2025). The multifunctional immune system. Science.

Shafqat, A., et al. (2023). How neutrophils shape the immune response: Reassessing their multifaceted role in health and disease. International Journal of Molecular Sciences, 24(24), 17583. https://doi.org/10.3390/ijms242417583

Wang, J., et al. (2024). Gut microbiota as a key regulator of intestinal mucosal immunity. Life Sciences, 345, 122612. https://doi.org/10.1016/j.lfs.2024.122612

This educational note was prepared from the lecture materials of Prof. Hussien Abouelhag (2010) and supplemented with current authoritative sources. It is intended for educational and publication purposes.

Data Availability Statement

No original datasets were generated for this review article. All cited data and findings are available within the original research publications referenced in the manuscript, accessible via the provided Digital Object Identifiers (DOIs) or through respective journal platforms.