This blog has been created partly as a companion to Chemistry for the Biosciences, the textbook that I co-author with Tony Bradshaw, and to act as an archive of posts I write for other sites (particularly the OUPblog). Like the book itself, it explores how life on the scale of atoms and molecules has an impact on biology - at the scale of cells, tissues, and organisms - and seeks to demystify a range of biological and chemical concepts.

The blog's name takes as its inspiration the cover of the first edition of Chemistry for the Biosciences, which depicts a gecko seemingly clinging to its surface. To find out what links geckos to chemistry, read this.

Saturday, 6 August 2011

How does our immune system work?

Each day of our lives is a battle for survival against an army of invaders so vast in size that it outnumbers the human population hugely. Yet, despite its vastness, this army is an invisible threat, each individual so small that it cannot be seen with the naked eye. These are the microbes – among them the bacteria and viruses – that surround us every day, and could in one way or another kill us were it not for our immune system, an ingenious defence mechanism that protects us from these invisible foes.

Our immune system is a multi-layered operation, much like the fortifications mounted to protect medieval castles. Our first line of defence – the equivalent of a castle moat – is our skin, a physical barrier that separates the hordes of microbes in our environment from the cells of our bodies that lie beneath. However, our skin does not keep us sealed off completely from our surroundings; indeed, some gaps in our defences are essential for our survival. And two gaps are very obvious: our nose and mouth. 

Every minute of every day we inhale air deep into our lungs. But along with the oxygen molecules we so desperately need come other less desirable particles, including viruses and fungal spores. Fortunately, we have another barrier in place to prevent these less desirable particles getting where we don’t want them. The lining of our lungs is covered by a layer of mucus, which traps many of these particles. Under this layer of mucus lie millions of tiny finger-like protrusions that bend from side-to-side, generating a Mexican wave-like movement that wafts this detritus-laden mucus up and out of our lungs, to be expelled (to put it as delicately as I can) every time we cough up phlegm or blow our noses.

Our requirement for food also leaves us exposed to the threat of invasion, this time via our digestive system. Once again, though, we are primed to defend ourselves. The inside of our stomach isn’t the most hospitable of places: it is highly acidic – perfect for aiding the digestion of food, but not a great place for many bacteria to set up home.

Despite the best efforts of these first lines of defence, however, the most determined invaders succeed in their mission and infect us. But this isn’t the end of the fight as far as our bodies are concerned: when our outer defences are breached a whole army of cells are in place to protect us. These cells are our white blood cells. 

The white blood cells operate as two separate battalions. One battalion is on the constant look-out for any general signs of trouble. In this respect, it acts a bit like a bouncer in a nightclub, who is primed to respond quickly and decisively to any one of a number of general ‘alarm’ signals - be it signs of a scuffle on the dance floor, or signs of inebriation from a late-night reveller. Whenever the alarm is raised inside the body, our first battalion is called to arms, and responds equally quickly and decisively, often simply by ‘eating’ whatever intruder first raised the alarm. 

This approach lacks what one might call any refinement: it is a fairly indiscriminate one-size-fits-all strategy. By contrast, the second battalion acts in a much more specific way, more akin to a group of snipers, each waiting for their particular target. This second battalion has two regiments – the B cells and T cells: B cells police the areas of the body outside of individual cells, including the blood; by contrast, T cells monitor the inside of cells. So how is the specificity of this second battalion achieved?

To answer this question, let’s focus on the B cell. B cells produce special Y-shaped molecules called antibodies. An antibody is like one half of a two-piece jigsaw: its specific shape allows it to recognise – and bind to – something with a complementary shape (just like neighbouring pieces of  a jigsaw fit together because their shapes are complementary). In the case of antibodies, however, the other piece of the jigsaw is a foreign object, such as a bacterium. The binding of an antibody to a foreign particle is one of the general alarm signals that call our first battalion to arms. So, the two battalions of white blood cell work together, with the second ‘sniper’ battalion often helping to focus the activity of the first on a particular invader.

Of central importance to the operation of our immune system is the fact that each B cell produces a uniquely-shaped antibody. Consequently, each antibody will recognize something different. This is important when we consider that our bodies face many different sources of danger, including many thousands of different microbes: we need lots of different antibodies to recognise them all. 

When we get infected by a specific type of bacteria, however, our bodies won’t be facing just one or two cells, but a whole army. We need lots of antibody to tag all of these invaders for destruction – but there’s no way we can always keep in circulation enough B cells to produce all the antibodies we need to destroy all the different microbes we might ever encounter. Instead, our immune system has a clever way of ensuring that large numbers of a particular antibody are only produced when actually needed. So how does this happen?

B cells circulate throughout our bodies in a continual surveillance mission, waiting until they encounter a foreign particle that can bind to their particular antibody (which, at this point in time, is protruding from the B cell like a probe). As soon as recognition happens, the B cell rapidly proliferates, stimulating the production of many copies of its particular antibody, which is now available in sufficient quantities to ‘tag’ many members of the invading army. This rapid proliferation is the reason why it feels like our ‘glands are up’ when we’re fighting infection: these ‘glands’ are our lymph nodes, specific areas around our bodies where B cells accumulate while they undergo proliferation; this accumulation occurs to such an extent that the lymph nodes actually swell.

The ingenuity of our immune system doesn’t end with the way it can detect many different foreign particles: it ‘remembers’ if it has encountered a particular invader before, and responds all the more rapidly (and effectively) if it encounters the same invader again. This memory is exploited by various vaccines, which ‘trick’ the immune system into thinking it is being attacked by a fully-fledged threat (when, in fact, it isn’t). When the body is subsequently exposed to the real threat, however, our immune system can mount a full-scale attack on the invader much more quickly than it could have done if encountering the invader for the first time. Indeed, the priming of our immune system by vaccines is essential to defend us against particularly nasty invaders, which could kill us if the immune system hadn’t already been primed.

This post leaves a number of questions unanswered. For example, is there a difference between bacteria and viruses, and what does this mean for how we defend ourselves against them? We’ll explore these questions in my next post.