Posts Tagged ‘ immunity ’

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.