Archive for the ‘ Immunity ’ Category

Adverse Immune Reactions

Below is the introduction and summary to this article, the full article includes information about the types of hypersensitivity (types I-IV) you can view and download it now for free at


The immune system has become adapted to ensure that ‘self’ cells are not subject to an immune attack. The body is able to do this because tolerance is developed towards self-cells, should this tolerance be broken down by some means, the host becomes subject to autoimmune attacks which can be potentially damaging.


Autoimmunity occurs when the body fails to recognise self-cells from non-self, this results in immune responses and damage to the tissue of the host. The variety of autoimmune responses can be split generally in to two groups; organ specific and non-organ specific. In autoimmune responses it is thought that either over reactive T-helper cells or deficient T suppressor cells are the cause. Autoimmunity can also be induced by reactions to a foreign antigen that then reacts with a self-antigen to invoke a response, for example infection with a minor bacteria (streptococcus) can lead to antibodies being produced against an antigen displayed on heart valves that would lead to cardiac problems. Autoimmunity is diagnosed by autoantibodies and the deliberate induction of autoimmunity has been used to control fertility and tumours (immunotherapy).


  • Autoimmunity – Inappropriate immune response to self antigens
  • Hypersensitivity – Overactive immune response to foreign and self antigens
  • Immunodeficiency – Ineffective immune response
  • Type I hypersensitivity – (IgE mediated, initiated in 2-30 minutes) Antigen induces cross-linking of IgE bound to mast cells with release of vasoactive mediators.
  • Type II hypersensitivity – (Antibody-mediated cytotoxic, 5-8 hours) Antibody directed against cell-surface antigens mediates cell destruction via ADCC or complement.
  • Type III hypersensitivity – (Immune complex mediated, 2-8 hours) Antigen-Antibody complexes deposited at various sites induces mast cell degranulation, neutrophil degranulation damages tissue.
  • Type IV hypersensitivity – (Delayed cell-mediated, 24-72 hours) Memory TH1 cells release cytokines that recruit and activate macrophages.

Immunity To Tumours

The second article of the day, the introduction is to this four page article is below. If this is what you were looking for please view the full article for free at The full article includes treatments, specific cell responses and the immune mechanisms.


A tumour is a swelling of part of the body caused by abnormal cell growth, this occurs when the normal cell division process becomes unregulated and cells proliferate uncontrolled. This results in cloned cells of the original defective cell, leading to a neoplasm – a new growth of tissue in the body that is abnormal. A tumour at a single site is known as a benign tumour, it becomes malignant (very virulent or infections and prone to reoccurrence after removal) when the tumour cells spreads to further sites within the body and begins to proliferate at these sites. Secondary malignant growths distant from the primary growth are known as metastases.

Not all tumours are cancerous, cancerous cells are damaged cells of the patients body that do not undergo apoptosis (programmed cell death), this means that their growth is no longer controlled and metabolism of the cells are altered.

Malignant tumours are named according to the tissue of origin:

  • Carcinoma – Arising in the epithelial tissue of skin or internal organs
  • Sarcoma – Arising in connective tissue or other non-epithelial tissue (mesenchymal cells)
  • Leukaemia – Arising in haematopoietic cells or blood forming organs such as bone marrow to produce abnormal leukocytes, these also suppress the production of normal blood cells
  • Germ Cell Tumours – Arising in reproductive tissues
  • Blastoma – Arising in embryonic tissues
  • Lymphoma – Arising in the lymph nodes

An early stage malignant tumour is called a premalignant tumour; premalignant tumours and benign tumours can often be treated with surgery alone. With malignant tumours this become much more difficult and other methods must be used in conjunction.

Immunity To Parasites

Remember, this post only includes the first page of the 3 page article, if this article is what you were looking for and you would like to read it in full, you can do so now for free at


A parasite is an organism which lives on or in another organism called the host. The parasite needs the host to live, but the host gains no benefit from having the parasite. The 3 main classes of parasite are protozoa (unicellular organisms), worms, and arthropods (insects and arachnids).

In comparison to acute bacterial or viral infections, a parasitic infection lasts much longer due to their well-evolved and effective methods of avoiding the immune system, a parasite is successful if it can successfully avoid or subvert immune responses directed against it. Many parasites are able to survive years in a host causing little or minimal harm, however for some parasites it is beneficial to cause disease in the host.

Parasites can cause harm to the host by:

  • Competing for nutrients in the host
  • Disrupting host tissue
  • Destroying host cells
  • Mechanical blockage

Endoparasties – Live inside the host

Ectoparasites – Live outside of the host

Protozoan Parasite Immunity

Protozoa are defined as single celled, eukaryotic microorganisms that lack cell walls. Not all protozoa are parasitic however.

Innate Immunity against Protozoa

Similar mechanisms to the removal of bacteria and viruses are in place to remove protozoa threats; this includes the complement system, NK cells and phagocytosis. However, many protozoa are breed and species specific, different species can be more susceptible to different pathogens.

Acquired Immunity against Protozoa

The acquired immune response to protozoa includes both humoral (antibodies, Helper T-cells and B cells) and cell mediated responses (Cytotoxic T-cells, macrophages, NK cells and cytokines).

Antibodies specific to protozoa surface antigens are released to control parasite numbers in the blood and tissues; this is aided by TH2 (T-helper 2 cells).

The cellular mediated immunity targets the intracellular infections and is mainly TH1 (T-helper 1 cell) driven. For the effective removal of most protozoa, the combination of TH1 and TH2 aided responses are required to target the protozoa at different stages of their life cycle.

Protozoa Evasion of Immunity

The mechanisms that protozoa have evolved to avoid the immune system are:

  • The avoidance of attachment and phagocytosis
  • Immunosuppression of the host immune system (e.g. destruction of T cells)
  • The blockage of antigen presentation (Expression in association with MHC Class II)
  • Alter surface antigens (Antigenic variation)
  • Block surface antigen expression to avoid detection (Parasite coats itself with host proteins)

Vaccinations to prevent possible protozoa infections have provided limited success, frequent boosters are needed and the vaccine must contain a mix of species and strains of protozoa to maximise its success.

Immunity Against Viruses


Viruses are small particles which infect living cells; this makes them obligate intracellular parasites. They have no reproductive mechanisms of their own so instead must use host cells to replicate. There are two main threats for a virus; the host’s immunity and the death of the host. Both of which will typically prevent the virus from propagating.

Many viruses are able to survive within the host for a long time without causing disease to the primary host. However when this virus is transferred to a secondary host, it is possible for a lethal disease to arise as a result. (An example is the transmission of the rabies virus to man). Vaccinating against the harmful effects of a virus therefore works best in the secondary host where the virus is not well adapted.

Structure of a Virus

Particles of a virus are known as virions. Virions encapsulate the nucleic acid core, which is surrounded by a layer of lipoprotein (or protein); this is known as the capsid. The degree of complexity of a virus can differ greatly. Viruses can contain either RNA or DNA and they can be either single stranded or double stranded, any combination of these still allows the virus (once in the host cell) to replicate.

Viral Pathogenicity

The virion is able to bind to a wide range of molecules to mediate attachment and internalisation by a host cell (by endocytosis). Once inside the cell, the capsid of the virion breaks down releasing the viral nucleic acid into the cytoplasm of the host cell. Once inside the cytoplasm, the viral nucleic acid is able to replicate and at the same time, it is also able to inhibit the production of DNA/RNA (thus protein synthesis) of the host cell.

Possible outcomes for a cell infected by a virus:

Lytic Infection – Host cell is destroyed, this is caused by virulent viruses

Persistent Infection – Host cell is not lysed, but virions are released slowly, over a longer period

Latent Infection – Occurs when there is a delay between the infection by the virus and the onset of symptoms

Transformation – Some viruses are able to transform a normal cell into a tumour cell

Immunity to Bacteria

Another article is up on, this one is about how the immune system deals with bacteria – Below is only the introduction, if you would like to read more then remember to check out the above ^^^


Bacteria exist naturally on many biological surfaces, for example the skin or the lining of the intestines. Bacteria like these make up the body’s natural flora and have a range of symbiotic relationships; a good example would be the flora of the rumen in cattle which degrade food materials, providing energy for both the cattle and the bacteria. The three main types of symbiotic relationship are:

•Mutualism – Both members of the symbiotic relationship benefit

•Commensalism – No apparent harm/benefit occurs to either member of the relationship

•Parasitism – One member of the relationship is living at the expense of the other resulting in disease

The pathogenicity of a certain bacteria depends on its survival inside the host – how well is it able to resist or evade host defence mechanisms and immune response. The resulting disease/damage caused to tissue is due to either the pathogenicity of the bacteria or the immune response of the host itself.

Bacterium Structure

Prokaryotes vs. Eukaryotes

Bacteria are prokaryotes, they differ from eukaryotic cells (such as those in humans) because the structures within prokaryotic cells are typically not compartmentalised. Prokaryotes also lack nuclear membranes, mitochondria, endoplasmic reticulum, a Golgi body, phagosomes and lysosomes (unlike eukaryotes). Also, prokaryotes only have a single, circular chromosome – unlike the nucleus of a eukaryotic cell.

Gram Staining

Bacteria can be very broadly categorised into two groups, gram negative and gram positive. This describes whether or not the bacterial will stain when using a gram stain. Gram-negative bacteria do not take up the gram stain; this is due to an extra outer membrane. Gram-positive bacteria do not have this extra outer membrane and so will take up the gram stain.

Bacterial Structures

•Plasmids – This is an extra-chromosomal strand of circular DNA, it is able to replicate independently from the main chromosome in the bacteria and the genes which the plasmid codes for aren’t typically essential for survival. The plasmid may be shared between bacteria which may be of concern as the plasmid often codes for pathogenesis and anti-bacterial resistance.

•Cell Envelope – This is the extra outer membrane seen in gram-negative bacteria

•Flagella – A protein organelle (consisting of flagellin) which is used for locomotion

•Pili (Fimbriae) – This is the organelle which allows adhesion to the epithelium of host cells.

•Capsules and ‘slime’ layers – These are layers outside of the cell envelope in some specialised bacteria. This extra layer allows the inhibition of ingestion by phagocytes as they are unable to detect the bacterium. A well-defined layer is known as a capsule, a lesser defined layer is known as a slime layer.

•Endospores – This is a term given to dormant forms of bacteria which are able to survive harsh conditions

Bacterial Immunity

This article can be found in full length at – Only the introduction is shown here


Bacteria exist naturally on many biological surfaces, for example the skin or the lining of the intestines. Bacteria like these make up the body’s natural flora and have a range of symbiotic relationships; a good example would be the flora of the rumen in cattle which degrade food materials, providing energy for both the cattle and the bacteria. The three main types of symbiotic relationship are:

  • Mutualism – Both members of the symbiotic relationship benefit
  • Commensalism – No apparent harm/benefit occurs to either member of the relationship
  • Parasitism – One member of the relationship is living at the expense of the other resulting in disease

The pathogenicity of a certain bacteria depends on its survival inside the host – how well is it able to resist or evade host defence mechanisms and immune response. The resulting disease/damage caused to tissue is due to either the pathogenicity of the bacteria or the immune response of the host itself.

Developing Immunity in New-Borns

The start if the article about new-born immunity is below, if you would like to see this in full then please remember to visit where you can also find a multitude of other articles and stories as well!


Any new-born animal is born from a sterile environment (e.g. a mother’s womb) into an environment which is filled with microbes and pathogens. Therefore it is important that the newly born animal is able to protect itself in its new, harsh environment. In most species (especially those with longer gestation periods) at birth, the immune system is well on its way to being fully developed but is not yet complete, taking some time (up to several weeks) to become fully functional.

For the immune system to develop, antigenic stimulation must occur, along with the development of antigen sensitive cells. This means that for the first few weeks of a new-borns life they are vulnerable to infection as their immune system is not yet complete. To overcome this, a temporary support system is provided by the mother. The mother is able to pass to her offspring antibodies and T-cells. These are able to temporarily support the animal whilst it builds up its own immune system. This is known as passive immunity.

The Developing Immune System

The development of the immune system in mammals as a foetus follows a consistent pattern. The initial lymphoid organ which develops is the thymus which is then followed by the secondary lymphoid organs (e.g. tonsils, Peyer’s patches, spleen, adenoids, skin etc.). The ability of the foetus to initiate a cell-mediated immune response develops around the same time as antibody production begins.


Here is the start of our most recent article, vaccination… to view/download/print this article head to as a shortcut you are now able to click the download button on the home page to download the most recent article, thus saving you from clicking through to the index.


There are two main types of immunisation, either passive or active immunity. Passive immunity being that derived naturally from a mother. A young animal will gain antibodies from its mother either during birth via the placenta or shortly after birth when the animal consumes colostrum from its mother. It is also possible to gain passive immunity by artificial means, this involves injecting an individual with an antisera (containing specific immunoglobulins). There are advantages and disadvantages of this artificial passive immunisation, the main benefit being that the resulting immunisation is immediately effective. The disadvantages include:

  • Temporary effect, lasting only until the Ig proteins are metabolised (a few weeks)
  • Only has an effect with diseases where an antibody response is the principle method of protection (as opposed to cell-mediated responses)
  • There is the possibility that hypersensitivity may arise from use of serums which have been obtained from foreign species
  • Induction of an active acquired immunity is blocked

The other type of immunisation is active immunisation, this is actively acquired immunity derived from either a natural infection or from artificial immunisation (inoculation with a weakened or dead organism).

Cellular Mediated Immunity

Ok so today you are getting a little more than the introduction… arent you lucky! But the premise is still the same, to view/download/print this article, please head to! Apart from that, id like to present: Cellular Mediated immunity! (Or at least 1 of the 6 pages)


The two major components of the adaptive immune system are known as cellular and humoral immunity. For an effective immune system these two branches of the adaptive immune system must interact. The main effector cells of these two systems are the T and B-lymphocytes.

T and B-lymphocytes both develop from a common progenitor in the bone marrow. T cells then move on to fully develop in the thymus and B cells develop in the bone marrow (in the foetus they develop in the liver). Any T or B cells that are at rest are morphologically indistinguishable.

Both T and C cells are able to recognise and bind an antigen and show a specific memory. B cells recognise antigens with the surface membrane Ig – which determines the specificity of the cell. T cells recognise the antigen with the T cell receptor which has both variable and hypervariable regions similar to yet still distinct from those of the immunoglobulin molecules.

Stimulation of a T cell by a specific antigen leads to the generation of effector T cells, which may directly and specifically kill cells bearing the appropriate antigen (or have other protective effects)

T and B cells can be distinguished by; their surface cells markers or their antigens. Many of these have a functional role e.g. CD8 are T Cytotoxic cells.

The Complement System / Cascade

As ever, below is only the introduction to this article. To review the article in its entirety please visit where you will find the full article for this and many similar articles under the “Learn” section. Hope this helps you:


The complement system or complement cascade as it is also known is a complex system of multiple proteins involved in inflammation and immunological response. The components of the complement system can be found throughout the body in fluids, providing the body with a systemic means of protection. Antibodies depend on complement for many of their biological activities.

Why is complement important?

  • It opsonises pathogens to promote phagocytosis by phagocytes which display receptors for complement
  • Certain components of complement act as good chemoattractants recruiting and activating phagocytes at the site of infection
  • Complement structures can cause cytolysis or damage to certain bacteria by puncturing their membrane

The important protein components of complement are number C1 to C9 (they are numbered in their order of discovery however and not their order of action as you will see later). Upon activation certain components may split into sub components, usually the small components are named with an ‘a’ e.g. C5a (these are the components which are able to diffuse through tissue readily) and the larger components with a ‘b’ e.g. C5b (these are the components which do not easily diffuse).

The complement system is known as a cascade because of the triggering and amplification of further components of the system. In the cascade once a component has been activated by a proteinase, the molecule itself which was activated becomes a proteinase for the next component of the cascade. The whole complement cascade can be triggered in its entirety in a matter of microseconds. During the activation process the smaller ‘a’ subcomponent peptides which are formed mediate many of the other effects caused by the complement cascade, for example acting as chemoattractants.

There are three types of complement cascade, the classical and alternative pathways and the Mannan-binding lectin pathway. Both provide a path to the cleavage of C3 which is a central event in complement activation.