The cells of the immune system are very strong lytic cells capable of causing severe damage to antigens, the antigens are made up of proteins, glycoproteins or polysaccharides; sometimes they are a combination of any two of these three molecules and might also consist of a combination of the three molecules, in fact it is normally this way as an antigens can also be a complete cell of either a microbe or a virus infected cell or a damaged cell or a neoplastic cell; but these are basically similar to the body cells. 

 ![image](https://img.esteem.ws/9j1a20tjkk.jpg)
The immune system consists of extremely strong lytic cells capable of destroying other cells. [Image source](https://commons.m.wikimedia.org/wiki/File:Cells_of_the_immune_system.jpg) wikimedia commons. File is free from known restrictions under copyright laws. 

Thus one would wonder why the body cells are not always attacked as seen in autoimmunity and hypersensitivity as the immune system which are made up of molecule, organs and cells which consists of proteins, glycoproteins and polysaccharide molecules are expected to also react with these normal body cells. 

The cell of the immune system have been naturally conditioned to recognise only abnormal cells and other molecular antigens, this keeps the normal body cells safe from the actions of these cells and the toxic substances they secrete in an attempt to protect the body from infections. This is a collaborative action as both the cells of the immune system and the antigens play a role in cell differentiation, the antigens display characteristics which differentiates them from the normal cells it compounds while the cell of the immune system response to these characteristics.
 
Here are the ways the antigens which infects the body simplifies their recognition :

**Immunogenicity**
 ![image](https://img.esteem.ws/m9dktgzw50.jpg)
Through the process of antigen presentation, immunogenic cells are delivered to the T-cells. [image source](https://commons.m.wikimedia.org/wiki/File:2216_Antigen_Processing_and_Presentation.jpg) wikimedia commons [Attribution
3.0 Unported](https://creativecommons.org/licenses/by/3.0/deed.en)

 Antigens and immunogens have been commonly used interchangeably; however, they are relatively different from each other with a marked relationship. Antigens generally speaking are substances or molecules which binds to the antibody receptors but do not necessarily initiate an immune reaction. Immunogens are ‘antigens’ which can bind to the antibody and also initiate an immune reaction; this is to say that all immunogens are antigens, but not all antigens are immunogens. Antigens which cannot initiate an immune response are termed ‘incomplete ’ antigens or Haptens.

Haptens were first used by Karl Landsteiner, they are low molecular weight compounds which binds to an antibody but cannot react with the products of the immune system, this may be drugs. Haptens can be made more immunogenic when they are complexed with a ‘Carrier protein ’ These are high molecular weight peptides which can increase the ability of a hapten to react with the products of immunity, they are related to Adjuvants which increases the intensity of an immune reaction by creating pores through which the antigens are released in bits, thus prolonging the persistence of the immunogen and increasing the local inflammatory reactions. 

Immunogenicity is the ability of an antigen to trigger an immune reaction, immunogenicity is a property of antigens/immunogens which differentiates them from the normal body cells or molecules which are non-antigenic. For a substance to be immunogenic; it must possess certain properties such as:

**A high molecular weight and size**: molecules of weight less than 100KDa are weak immunogens, and hence may be unable to trigger noticeable reactions; this is no absolute however as many molecules of lower molecular weight have been shown to be strongly immunogenic. 

**Degradability and susceptibility to antigen processing and presentation**: Antigen processing is a process undertaken by the cells of the immune system to breakdown antigens into peptides which can be recognized by the Major Histocompatibility Complex. The Major Histocompatibility Complex (MHC) molecules are molecules synthesized by the antigen presenting cells which binds to these processed antigens and presents them to the T-cells, the T-cells only recognizes antigens which are complexed with the MHC molecules, this is also a means of protecting the normal cells from the actions of the T-cells. Hence for an antigen to be immunogenic; it must be susceptible to these antigen presenting cells and should be degradable by them too. Heterogeneity and complexity also increases immunogenicity as complex and heterogeneous molecules are more likely to cause an immune reaction, their level of complexity and immunogenicity also plays a role in the intensity of the reaction they initiate.

**Pattern display**
 ![image](https://img.esteem.ws/srdcq5w1u7.jpg)
Patterns displayed by immunogenic cells triggers immune response [image source](https://en.m.wikipedia.org/wiki/File:Effector_Triggered_Immunity.tif). Wikimedia commons. [Attribution-Share Alike 4.0
International](https://creativecommons.org/licenses/by-sa/4.0/deed.en)

 Immunogens also display certain abnormal patterns either in their external skeleton or their cytoplasm. These patterns makes them different from the normal body cells and hence enables the immune system to recognize and mark them as different from the normal cells. Pathogens display patterns called the ‘Pathogen Associated Molecular Patterns’ (PAMPs) , this seen in gram negative and gram positive bacteria, viruses and other pathogenic cells. Viruses possesses single stranded DNA; this is not seen in many other normal molecules and this differentiates viral molecules from the normal cells. Gram negative bacteria cells posses cell walls made up of lipopolysaccharides also known as the Endotoxins, this also differentiates them from gram positive bacteria which posses peptidoglycan cell walls, hence these patterns not only differentiates immunogens from the normal cells but also differentiates them from other immunogens, the immune system is able to detect not only the immunogen but it’s form, type and immunogenicity. 

Damaged cells in the body also displays certain configurations called the ‘Damage Associated Molecular Patterns’ (DAMPs),  for the immune system to mark a cell as damaged, the cell must be manipulated or damaged to the extent of displaying these patterns. Damage Associated Molecular Patterns includes molecular Serum amyloid A (SAA) and high mobility groupbox-1 (HMGB-1); high mobility group box-1 is produced by the cells under stressed condition, hence stressed out cells may be marked as damaged. The serum amyloid A is produced in response to injury, inflammation and infection. This differentiates normal cells from pathogens or damaged cells and keeps the normal cells away from destruction by the immune system. 

Immunogenicity and patterns display are the major ways through which the immunogens enables their recognition and simplifies their detection and subsequent elimination by the cells of the immune system. The immune system also device means of responding specifically to these immunogens via the following means:

**Immunocompetence**

This is the ability of the T-cells to differentiate self from non-self antigens. The T-cells are produced are produced in the bone marrow but are transported to the thymus, a bi-lobed encapsulated organ located above and in front of the heart. In the thymus, the T-cells are positioned so as not to encounter any antigen, this is to avoid the cells getting contaminated by the antigens; they are trained to be able to recognise the normal self antigens and differentiate them from the non-self antigens. The T-cells that fails to develop immunogenicity are destroyed, this explains why the T-cell releases little amount of cells compared to its rate of mitotic division. This action protects the body from autoimmunity as the cells which are not immunocompetent will eventually attack the normal cells. In the thymus, the T-cells are also differentiated into Helper T-cells (CD4+) and cytotoxic suppressor T-cells (CD8+), these cells perform regulatory and cytotoxic roles in the T-cell mediated immune reactions, hence the name ‘thymus-derived’ cells. 

**Pattern recognition**
 ![image](https://img.esteem.ws/7pv83yxitj.jpg)
Polymeric immunoglobulin receptor. [image source](https://en.m.wikipedia.org/wiki/File:Protein_PIGR_PDB_1xed.png) wikimedia commons [license:Attribution-Share Alike 3.0 Unported](https://creativecommons.org/licenses/by-sa/3.0/deed.en)

The T-cells contains receptors which are able to recognize certain patterns displayed by the pathogens and damaged body cells, these receptors are also able to antigens bound to the Major Histocompatibility complex molecules. Other cells of the immune system are also able to recognize the FC regions of the Immunoglobulins and also the complement system; the receptors includes :

**FC receptors** : Different antigens binds to the hypervariable regions of the Immunoglobulins, the FC regions of the immunoglobulins is tasked with conveying information about these bound antigens to the effector cells or the complement system. In the antibody dependent cell mediated cytotoxicity, the cells of the immune system which have affinity for this FC regions are cross-linked with it via the FC receptors displayed on their membrane. Recognition of the FC regions of the Immunoglobulin G results in a more intense response to an already encountered immunogens in anamnestic reactions, recognition of FC regions of Immunoglobulin E results in hypersensitivity. 

**Complement receptors** : The complement protein 3 of the complement system coats bacteria and other immunogens, the phagocytic cells displays receptors that binds to these complement 3 coated bacteria. The complement proteins are also mediators of inflammation and can also act on their own to lose antigens through the membrane attack complex. 
**Scavenger receptors** : Non-specific binding of the phagocytic cells to immunogens may also occur due to the polyanion and bacteria particles, this initiates phagocytosis and subsequent elimination of the immunogen.
**Toll-like receptors** : These mediates the innate immunity, the binding of the Toll-like receptors initiates inflammation, phagocytosis and the release of cytokines. Toll-like receptors in the body recognize these pathogen associated molecular patterns and humans have about twelve (12) (numbered TLR1-12) which recognize different patterns displayed by the immunogens. The TLR4 recognises the Endotoxins or the lipopolysaccharides of the gram negative bacteria cell wall; TLR3 recognizes the double stranded DNA of the bacteria, TLR2 recognizes the peptidoglycan cell wall of the gram positive bacteria, hence the innate immune system is able to differentiate non-self and self antigen and does not react to the healthy and normal cells 

**Clonal anergy**
 ![image](https://img.esteem.ws/x05aapnmnm.jpg)
Process of clonal deletion. [image source](https://en.m.wikipedia.org/wiki/File:Clonal_Deletion.png). Wikimedia commons [Attribution-Share Alike 4.0
International](https://creativecommons.org/licenses/by-sa/4.0/deed.en)

When the Immunoglobulin membrane receptors binds to an antigen, they stimulate the synthesis of many antibodies which are identical to the stimulating antibody, this leads to the production of a large number of antibodies to fight an immunogenic cell. All these antibodies are not involved in this defense process and may as a result attack the normal self  antigens and the body cells. The immune system as a result developed a means by which these excess antibodies can be rendered harmless to the body, the specialized mechanism through which the immune system reduces the amount of active clones of immune cells is known as Clonal anergy, this is not only seen in the B-cells as the T-cells also exhibits this feature. 

When adequate number of antibodies are produced, the lymphocyte control system stops the further production of antibody clones and decreases the concentration of the membrane bound antigens; the antibodies are anergized by exposing them to antigen. In the T-cells, the binding of the T-cells to MHC molecules which do not express the co-stimulatory signals anergized the T-cells. 

**Conclusion**. 

The body system not only protects us from infections, but it also protects us from itself, autoimmunity only occurs when there is a failure in any of these processes, here these regulatory processes cannot be performed by the immune system, resulting in the immune system destroying the body’s own cells. 

If the above processes are not faulty, the immune system does not attack the body cells, autoimmunity only results from a malfunction in any of these process, antigenic variation makes the immune system’s response to antigens more tedious as the antigens keeps changing its form, this is seen in parasitic attacks such as trypanosomiasis or sleeping sickness, the antigens changes form and as a result the immune system would have to re-adapt to a new form of antigen each time this is just one of the instances where the antigen’s features affects the body’s response to them. 

The receptors of the immune system sometimes could develop errors in an attempt to detect the exact antigen which leads to the presentation of the normal body cells to the immune system the receptors of the immunoglobulins and the major histocompatibility complex determines the accuracy of the adaptive immune system and hence a defect here results in an overall faulty immune response. 

**REFERENCES**
1.[Clonal synergy~Wikipedia](https://en.m.wikipedia.org/wiki/Clonal_anergy)
2.[polymeric immunoglobulin receptor~Wikipedia](https://en.m.wikipedia.org/wiki/Polymeric_immunoglobulin_receptor)
3.[pathogen associated molecular  patterns ~Wikipedia](https://en.m.wikipedia.org/wiki/Pathogen-associated_molecular_pattern)
4.[Damage associated molecular patterns~wikipedia](https://en.m.wikipedia.org/wiki/Damage-associated_molecular_pattern)
5.[Clonal anergy: Why you don't fight yourself~steemit](https://steemit.com/stemng/@henrychidiebere/clonal-anergy-why-you-don-t-fight-yourself)


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