The immune system coordinates a complex array of components consisting of specialised organs, cells and proteins. On the surface, the primary role of the immune system in defending the body against infectious pathogens might appear straightforward. This begs the question: why is the immune system so complicated?

There are a number of reasons for this degree of complexity. The first is that the immune system evolved to fight pathogenic infection while minimising collateral damage to healthy tissue. For sake of argument, if the lungs of a patient were infected with a pathogenic microorganism, the immune system could release molecules that would kill the pathogen. However, if these molecules were to be released in an uncontrolled and directionless fashion, healthy tissue would be destroyed too.

This analogy raises another important feature of the immune system, namely, the recognition of differences between healthy cells and pathogens referred to as ‘self’ and ‘non-self’ respectively.

Each one of us has a personal army of immune cells that are programmed to harmoniously communicate with one another ensuring discrimination of self from non-self and efficiently respond to infection. Inflammation is a key process that ensures the recruitment of immune cells and proteins to the site of infection.

Among these are killer immune cells and antibodies that specifically neutralise pathogen-associated molecules called antigens. Once the pathogen is eliminated, other immune cells play a key role in restoring normal conditions by promoting tissue repair processes.

In autoimmune disorders, rogue immune cells fail to recognise healthy tissue as self and attack it. Among such disorders are psoriasis, lupus, rheumatoid arthritis, multiple sclerosis, Crohn’s disease and type I diabetes. Overall, they affect 5 per cent of the population in industrialised countries.

Autoimmune responses resemble normal immune responses but are initiated by self-antigens rather than pathogen-associated antigens. The human body has evolved a multitude of checkpoints that prevent the immune system from attacking healthy tissue. Together, these checkpoints must act concertedly to strike a delicate balance of dampening autoimmune responses while maintaining the ability of the immune system to strike against pathogenic infection. Indeed, it is quite common to observe isolated breakdown of one of these checkpoints in healthy individuals without any clear consequences.

Autoimmunity occurs when there is a collapse of enough checkpoints resulting in sustained reaction to self-antigens ultimatelyleading to tissue damage. In autoimmunity, self-antigens are not eliminated by the immune system. The constant presence of self-antigen leads to a salient feature of autoimmune disorders called chronic (sustained) inflammation, which leads to a continuing self-destructive process. Both auto-antibodies and killer cells directed at self-antigens participate in this immune mediated tissue damage.

The focus of my research is, therefore, directed at understanding how immune cells recognise antigens and communicate effectively with one another. Understanding these events is relevant in developing future therapies where the immune system plays a central role and intervention can help balance its response to disease.

David Saliba is a senior lecturer in the Department of Applied Biomedical Sciences, Faculty of Health Sciences at the University of Malta and also holds an honorary research fellow position at the Kennedy Institute of Rheumatology at the University of Oxford.

Sound bites

• Identifying the cause of auto-immune disorders.  While we understand the complex mechanisms that result in autoimmunity, intense research by the scientific community is directed at identifying the root cause of each of these disorders. In recent years, it has become clear that both genetic and environmental factors contribute to the development of autoimmune disorders. Genetic studies have identified multiple genes that contribute to increased susceptibility to autoimmune diseases. On the other hand, it is much more difficult to identify environmental influences. This is partly due to the chronic nature of these disorders. It is hard to pinpoint exactly when the autoimmune response began and therefore challenging to determine the single or combination of environmental triggers.

• Imbalance in gut flora linked to Rheumatoid arthritis. The intestinal gut flora is an intricate world of microbes that has important implications in proper development of the immune system. Alterations of non-pathogenic microbial populations are often associated with immune disorders, particularly of the autoimmune kind. Rheumatoid arthritis is a debilitating disease since it primarily affects the hands, wrists and synovial joints. Scientists have compared faecal microbes of healthy individuals to rheumatoid arth-ritis patients. These studies have evidenced a clear shift in microbial populations demonstrating that specific microbial species may be responsible for the onset and progression of rheumatoid arthritis. It will be exciting to see how this field shapes the development of novel therapeutic approaches and biological markers of this disease.

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