The Wednesday Post (10/11/10)

We try to not be alarmist here at Disease of the Week but two papers were brought to my attention by a PhD student in the discipline (this one and this one). The first response to a new paper should be that the researchers have moulded the current understanding and made some new insights. I have never approached reading papers this way, to my own detriment it must be noted. I always expect each and every paper to have changed the world.



Perhaps not so much.


Let me explain. One of the central tenets of immunology as proposed by Sir Frank Macfarlane Burnet is that each lymphocyte contains an individual and specific receptor that allows it to selection based on the appearance of its specific and individual epitope. This specific interaction allows the immune system to only expand cell populations that can respond to the particular invader and not others, also known as the theory of clonal selection and expansion.

This is very important stuff. Introduced in first year biology classes and elaborated as a central theme for the rest of your immunology degree level important stuff.

Well these papers by researchers at the Australian National University (ANU) have found that lymphocytes can share surface receptors…

What the what?!?

These researchers have observed both T and B cells undergoing receptor sharing.

This finding initially didn’t make sense to me as the production of a specific receptor is a very controlled process and in the end links a receptor to the genetic machinery required to produce more of that receptor if required. If cells can share the receptors how do they know how to make more of that receptor? They cant! So why? ARGHHHHHH!!!

Clonal expansion of lymphocytes: 1. Hematopoietic stem cell 2. Immature lymphocytes with various receptors 3. "Self"-antigens from the body's own tissues. Positive interaction here result in induced cell death 4. Mature, inactive lymphocytes 5. Foreign antigen. Positive interactions here promote cell growth and division 6. Cloned activated lymphocytes


The researchers propose this as a very specific mechanism that occurs during he upregulation of an acquired immune response. In the case of B cell receptor transfer they suggest that the transfer of receptors allows bystander B cells which would otherwise be doing nothing to present antigen to CD4+ T cells. CD4+ T cells are also known as helper T cells and are involved in the release of immune chemicals known as cytokines and chemokines that further a B cell response.

In the case of T cell receptor sharing they suggest that the transfer of the active T cell receptors from CD8+ T cells to other surrounding CD8+ T cells may result in a transient increase in the population of cells able to induce apoptosis in virally infected cells during an infection but the recipient cells probably can not induce clonal expansion.

Whilst I flipped out a bit earlier these studies MAY represent an interesting rethink in the development of an immune response, or they may be interesting anomalies. At this stage its too early to tell but if this is real its very interesting. Or at least I think it’s interesting. Maybe I need to get out more.


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Chaudhri, G., Quah, B., Wang, Y., Tan, A., Zhou, J., Karupiah, G., & Parish, C. (2009). T cell receptor sharing by cytotoxic T lymphocytes facilitates efficient virus control Proceedings of the National Academy of Sciences, 106 (35), 14984-14989 DOI: 10.1073/pnas.0906554106

Quah, B., Barlow, V., McPhun, V., Matthaei, K., Hulett, M., & Parish, C. (2008). Bystander B cells rapidly acquire antigen receptors from activated B cells by membrane transfer Proceedings of the National Academy of Sciences, 105 (11), 4259-4264 DOI: 10.1073/pnas.0800259105



Filed under James' Corner

2 responses to “The Wednesday Post (10/11/10)

  1. It’s interesting, no doubt of it, but it’s not such a huge surprise. It’s a continuation of an observation from the early 2000s that showed receptor swapping between antigen-presenting cells and T cells. Now that was a big surprise, and there was a lot of skepticism, but there have been more and more examples over the years, and this seems to be more of the same. There hasn’t been as much evidence of biological importance (a much harder problem to address). These papers are, as I say, interesting and potentially important, but not as groundbreaking as all that.

    • You’re right but I had never heard about it until recently as I concentrate more on the bacteria and less on the host normally. Until I read the papers though I couldn’t understand a situation where receptor sharing would be beneficial as the associated somatic hyper-mutation no new extra antibodies can be made. These papers clarify that point a little for me but I wonder if the same thing would be seen by accident if the cells are fusing or if there is some other mechanism at play. Interesting stuff either way.

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