Humoral Immunity
Definition and Primary Functions
Humoral immunity is an immune response mediated by soluble host proteins called antibodies or immunoglobulins. It provides the first line of defence against a wide range of invading foreign substances.
- It is directed primarily against extracellular bacteria.
- This includes exotoxin-producing bacteria such as Corynebacterium diphtheriae and Clostridium tetani.
- It also targets bacteria whose virulence is due to polysaccharide capsules.
- Examples include Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae.
- It protects against certain viruses that infect the respiratory or intestinal tract.
- It prevents the recurrence of viral infections.
- It participates in the pathogenesis of type I, II, and III hypersensitivity reactions and certain autoimmune diseases.
Mechanism of Antibody Production
The production of antibodies is the main feature of the humoral immune response. It depends on a complex interaction between macrophages, helper T-cells, and B-cells.
Functional Limbs
- Afferent limb.
- It involves antigen entry, its location in tissues, and contact with suitable immune cells.
- Central function.
- It involves antigen processing and the control of antibody production.
- Efferent limb.
- It consists of antibody secretion, distribution in tissues and body fluids, and manifestation in combating the pathogen.
Cellular Interaction
- Antigen-presenting cells such as macrophages and dendritic cells process the antigens.
- Antigen fragments appear on the surface of macrophages in association with Class-II Major Histocompatibility Complex proteins.
- This complex binds to specific receptors present on the surface of helper T-cells.
- These helper T-cells produce cytokines that activate B-cells.
- The activated cytokines include interleukin-2, interleukin-4, and interleukin-5.
- The activated B-cells undergo clonal proliferation and differentiate to form plasma cells.
- These plasma cells then produce specific immunoglobulins.
- T-cell-independent antigens can activate B-cells directly without the help of T-cells.
- These antigens induce only the production of IgM antibodies.
- B-cells require interleukin-4 and interleukin-5 to switch classes to produce IgG, IgA, and IgE.
Phases of Antibody Production
The production of antibodies follows a characteristic pattern.
- Lag phase.
- This is the immediate phase following exposure to the antigen where no antibodies are detected in the circulation.
- Log phase.
- This phase is characterised by a steady rise in antibody titres in the circulation.
- Plateau phase.
- This is a phase of equilibrium between antibody synthesis and catabolism.
- Phase of decline.
- This phase is characterised by an increase in antibody catabolism compared to antibody production.
- It leads to a fall in antibody titre in the circulation.
Primary and Secondary Immune Responses
Humoral immune responses are divided into primary and secondary responses based on the sequence of antigen exposure.
| Feature | Primary Immune Response | Secondary Immune Response |
|---|---|---|
| Lag Phase | Usually long, lasting weeks or months. | Very short, typically 3 to 4 days. |
| Antibody Production | The amount of antibody production is relatively low. | High levels of antibody production are seen. |
| Antibody Isotype | Induces IgM antibody production primarily. | IgG antibody predominates. |
| Duration of Titre | Reaches the phase of decline relatively early. | Remains high for a longer time. |
| Cell Type | NaΓ―ve B-cells are involved in antibody production. | Memory B-cells are involved in antibody production. |
| Antigen Dose | A relatively high dose of antigens is required. | A low dose of antigens is sufficient. |
Effector Mechanisms of Antibodies
Antibodies confer protection against infectious pathogens through specific biological mechanisms.
| Mechanism | Description of Action |
|---|---|
| Neutralisation | Antibodies bind to the pathogen or foreign substance. This blocks the binding of the pathogen to host target cells, making it ineffective. |
| Opsonisation | Antibodies bind to the pathogen to assist in its uptake by phagocytes. Fc receptors of phagocytes interact with the Fc region of the coating antibody. |
| Complement Activation | Antibodies activate the complement cascade to effectively kill certain bacteria and viruses. Pathogens can also be opsonised by complement components like C3b. |
Factors Influencing Humoral Immunity
Many factors affect the production of antibodies and the humoral immune response.
- Genetic factors.
- The immune response gene controls the differences between responders and non-responders.
- Age.
- The embryo and infant are not fully immunologically competent.
- Full competence for IgG is achieved by the age of 5 to 7 years.
- Nutritional status.
- Deficiencies of amino acids and vitamins decrease the production of antibodies.
- Antigen administration.
- Parenteral administration of the antigen induces a better immune response than oral or nasal routes.
- A minimum critical antigen dose is essential to elicit an optimum immunological response.
- Adjuvants.
- These are substances that enhance the immunogenicity of an antigen.
- They delay the release of an antigen from the injection site to prolong the antigenic stimulus.