All About Immunization vs vaccination!

Table of Contents

IMMUNITY

Immunity origins

• The word “immunity” is derived from the Latin immunis, meaning exemption from military service or public services
• It is defined as the “ability of an organism to recognize and defend itself against specific pathogens or antigens.”
• Burnet and Medawar, the curious Nobel Prize winners of 1960,
  • were recognized for conceptualizing “self” and “non-self,”
  • which entailed that the human body had learnt to tolerate its own tissues (as self) but was intolerant to foreign tissues (as not-self).
  • Thus, under normal circumstances,
    • the body tolerates its own tissues (immunological tolerance)
    • recognizes and destroys (“non-self”) foreign tissues.
• In the modern sense, therefore, immunity has been defined as
  

  the ability of the body to recognize, destroy, and eliminate antigenic material foreign to it.

• Immunization has to lead to;
  • eradication of smallpox,
  • elimination of poliomyelitis
  • elimination of neonatal tetanus,
  • a marked decrease in the incidence of diseases like
    • polio,
    • diphtheria,
    • pertussis,
    • tetanus,
    • measles

Infection and its effects.

• The phenomenon of infection may be compared to a home invasion.
• The immune response is akin to the safety precautions undertaken by the legitimate owner.
  • The infectious agent originates from infection specific source/reservoir
  • It gains access to a susceptible host through its preferred portal of entry.
  • The host repels the onslaught through the first line of defence at this juncture utilizing the non-specific Native or Innate Immune mechanisms.
  • After penetrating the host’s innate immunity barrier, the infectious agent attaches itself to targeted specific host cell receptors by its surface proteins and gains entry into the host cells.
  • This entails a more robust Adaptive pathogen-specific immune response which constitutes the second line of defence.
  • The detection of foreign surface proteins on the infectious agent triggers a specific immune response.
  • Pathological changes
    • cellular lysis due to a multiplication of the agent within the host cell
    • toxin-mediated damage to the host cell
    • the detrimental effect of the host immune response itself.

Non-Specific | Innate immunity

• These are generic defence mechanisms;
  • tears, saliva, gut acidity and other gastrointestinal tract secretions
  • They create conditions that neutralize a variety of infectious agents.

• Similarly at a cellular level non-specific leukocytes, macrophages, as well as chemicals like kinins, are released in a general response to any kind of infectious agent

• Accordingly, innate immunity is constituted by several sub-strategies.

  1. Physical barriers against infection – The skin (integumentary system) and mucous membranes(with superimposed physiological defences created by the ciliary motion of mucus) act as a continuous barrier surface, which must be breached by any pathogen before entering the human body.

  2. Physiological limitations such as pH, temperature, and oxygen tension limit microbial growth.

  3. Enzymes like lysozyme secreted into external body fluids also resist invasion. Soluble factors within circulation such as complement, interferons, and C-reactive protein are of importance in defence against infection.

  4. Phagocytic cells- Macrophages and polymorphonuclear leukocytes (PMN) can recognize bacterial and yeast cell walls through broadly specific receptors (usually for carbohydrate structures), and this recognition is enhanced by complement activation(opsonisation).

Specific Immunity

• Characterised by pathogen identification and a specifically targeted response.
• Specific immunity is constituted by humoral components (antibodies) and cellular components (such as T and B lymphocytes)
  

  Active immunity

• Specific immunity actively mounted and sustained by the host is termed as Active immunity.

  • It could be acquired by hosting a particular infectious agent and mounting a specific immune response in due course of nature
  • artificially by way of administering vaccines.

  Passive immunity

• Immunity passively “gifted” by an external source—termed as Passive immunity.
• It could be acquired naturally via the transfer of maternal antibodies to the child in utero or through breast milk.
• May be acquired artificially by administering immunoglobulins.

Host Defenses

There are two different types of host defences on antigen exposure, classified based on the primary mechanism involved. These are:

1. Humoral immune response, which involves activation and clonal selection of B-cells, resulting in the production of antibodies
2. Cell-mediated immune response, which involves activation and clonal selection of cytotoxic T-cells

The sequence of events

1. The pathogen is engulfed by an antigen-presenting cell (APC) at the portal of entry.
2. It undergoes lysis by lysosomal enzymes and the antigens get sieved out
3. The antigens are taken up by Major Histocompatibility Complex(MHC) molecules to the cell surface.
4. The antigens presented by the APCs activate the T lymphocytes around them.
5. The activated T-lymphocytes convert into Cytotoxic T-cell (Tc) & T-helper cells (Th).
6. The Th cells sensitize B-Lymphocytes to undergo clonal selection and produce specific antibodies.
7. The Cytotoxic T-cell mediate Cell-mediated immune response.

Humoral Immunity

• An activated B-cell specialise into an antibody-secreting Plasma cell and memory B-cell.
• When the host is exposed to a new antigen, the initial immune response also termed as primary immune response takes 7–10 days.
• The primary response is the elevation of pathogen specific-IgM within 7–10 days
• This is followed by a specific-IgG response seen 3–4 weeks after infection.
• The specific antibodies bind to antigens on the pathogen and eliminate them by the way of phagocytosis or complement-mediated mechanism.
• The memory B-cells remain dormant and undergo maturation over 4–6 months.
• During this process, the mutations allow for an increase in the affinity of the specific antibody.
• When the host is exposed to the same antigen for a second time, the memory B-cells are activated within a short duration, i.e., within 24 hours.
• This is termed a secondary immune response.
• The secondary response exhibits the following features:
  • Shorter lag time
  • Rapid buildup
  • The higher overall level of response
  • More specific or better “fit” to the invading antigen
  • Utilization of IgG instead of the large multipurpose antibody IgM

Active vs passive immunity

• Humoral immunity is active when the organism generates its own antibodies, and passive immunity is active when antibodies are transferred between individuals.
• Similarly, cell-mediated immunity (CMI) is active when the organisms’ own T cells are stimulated and passive when T cells come from another organism.

Cell-Mediated Immunity

• Macrophages engulf antigens and process them internally.
• This sensitizes the T cells to recognize these antigens.
• T cells are primed in the thymus, where they undergo two selection processes.
  • The first positive selection process weeds out to only those T cells with the correct set of receptors that can recognize the MHC molecules responsible for self-recognition.
  • Then a negative selection process begins whereby T cells that can recognize MHC molecules complexed with foreign peptides are allowed to pass out of the thymus.
• Cytotoxic or killer T cells (CD8+) do their work by releasing lymphotoxins, which cause cell lysis.
• Helper T cells (CD4+) serve as managers, directing the immune response.

Local Immunity

• Local immunity is believed to be produced
  • by fixation of various specific humoral antibodies in tissues and cells, or
  • it may be a non-specific response of local tissues induced by a local application of antigen,
  • against a subsequent infection threatening systemic disease,
• for example, the oral polio vaccine (OPV) is used for producing immunity against poliomyelitis.

Types of Immune Response

• The first encounter with an antigen is known as the primary response.
• Re-encounter with the same antigen causes a secondary response that is more rapid and powerful.
  • The immune response depends on the following factors:
  • Nature and dose of antigen
  • Route of administration
  • Type of adjuvants used
  • Nutritional status of the recipient