Feature: Immunity at Defcon B

Robert Brink.

This feature appeared in the November/December 2009 issue of Australian Life Scientist. To subscribe to the magazine, go here.

Robert Brink is an immunologist, and like most of his kind, he barracks for one of two teams: B cells or T cells. In Brink’s case it is B cells (and make sure you don’t accuse an immunologist of barracking for the wrong one), which are white blood cells charged by the immune system with producing antibodies against foreign antigens, such as those expressed by viruses and bacteria (and the immune system is not fussy whether the invaders are coming in by water or air). The ultimate job of these cell types is to produce antibodies that can eliminate the bad guys and either prevent or cure an infection.

Brink’s research group at the Garvan Institute of Medical Research in Sydney is particularly interested in the complex process by which B cells function to fight off an infection and in nutting out the decisions made by the immune system along the way, and he’s speaking at the Australasian Society of Immunology meeting on the Gold Coast in December.

A lot happens between the immune system detecting a foreigner on their shores and getting rid of it, and at ASI, Brink will map out the steps of this process – as observed in their in vivo model – and also talk about some exciting new findings regarding those B cell lifestyle decisions.

Flying under the radar

According to Brink, an age-old problem is actually ‘seeing’ this invasion and B cell defence process as it happens from beginning to end – mainly because of the way the immune system is set up.

“Essentially there are zillions of these immune cells floating around that are basically all the same except for the antigen receptors on the cell surface. The gene events that control the antigen specificity demonstrated by B cells in the first place are set from birth, and the result is an incredible diversity built into the antibody receptors so that our immune system can handle most of the antigens thrown at it over a lifetime.”

The flip side is that with such a spectrum of antigen-recognition specificities, the number of cells that can produce just the right antibody to recognise an invading molecule is small, and insufficient to mount an immediate and fully effective antibody-based defence against the threat. These cells need to be expanded, and when activated by the foreign antigen they go off and proliferate to produce an army of copies or ‘clones’ with the desired specificity.

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