About

AnneSp1My name is Anne Spurkland. I am a professor of medicine at the University of Oslo. I teach anatomy and do research within immunology and autoimmune diseases. Immunology is about the body’s defence against all external and internal threaths. Immunology is therefore a field that involves nearly all aspects of body and health. The aim of the blog ImmuneGlimpse is to give small glimpses into the workings of the immune system. The blogposts presented here in English will generally have been published first in Norwegian on my Norwegian blog ImmunGlimt.

From time to time I will write about a topic that is also in the news, but most often it will be small pieces of information that I find are interesting examples on how the immune system works. I will present both well established and more recent knowledge.

I will make the illustrations by hand, as I would have used blackboard and chalk for a student lecture. Be aware that this is to be seen as “caricatures” where the sizes are not comparable to each other. All molecules that I will write about are so small that they are not visible, even in the microscope, while on my drawings they will become super-sized! This is how we who work with molecules on a daily basis manage to relate to something which is not visible. We draw molecule-caricatures.

Feel free to send me comments via the blog, with questions or suggestions for topics to write about. Although the blog originally was written in Norwegian, I will of course also welcome comments from readers of the English version of the blog.

Blogpage by Anne Spurkland translated from Norwegian, 24th November 2014.
First Version published 28th July 2012

4 thoughts on “About

  1. Hi Anne, I have a question about having autoantibodies such as antimyelin antibodies, Antiphospholipid antibodies, antithyroid antibodies.
    How can this be related to having congenital Common Variable Immune Deficiency (CVID) and defective B cells. The B cells are ‘naive’ and unable to recognize viruses, bacteria, etc. The treatment for this is to get IVIG infusions every 4 weeks. How can an immune system go so wrong?

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      • Hello again

        This is a very interesting question, that also immunologists are puzzled by. How come that autoimmunity can occur in the presence of immunodeficiency. Again, it may have to do with disturbed information transfer within the B cell.

        Each B cell has an antigen receptor that has been made by random combination of short gene segments. Sometimes these rancomly generated antigen receptors can bind to proteins and structures found within the body itself. To avoid autoimmunity, such B cells are rendered inactive or are eliminated. The elimination of auto-reactive B cells is dependent on adequate transfer of signals from the cell surface to the cell interior.

        If the transfer of signals within the B cells is perturbed, resulting in CVID and lack of ability to respond to viruses or bacteria, this signaling defect will also affect auto-reactive B cells. Instead of being elminated, auto-reactive B cells may remain in the body. Over time, some of these B cells will produce sufficient amounts of auto-antibodies. This may give clinical symptoms of autoimmune disease.

        Anne S

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    • Hello again

      I am sorry for this very late response. Your comment has slipped under my radar till now. The last year or so I have been very busy promoting my newly published book about the immune system (still only available in Norwegian): Immune. The body’s eternal struggle to survive.

      The cause of CVID is not known. A B cell that remains naive and does not recognize viruses, bacteria etc may have a problem with transfer of signals from the cell surface to the cell interior. It is only when information from the outside of the cell is relayed to the inside, that the decision to divide and start to produce antibodies can be made.

      In order to become activated, a B cell also needs signals coming from T cells, specifically an activated T cell that react to the same virus or bacterium. In order for the B cells to get this help from T cells, the B cell needs receptors on the surface that can interact with corresponding molecules on T cells. In some CVID patients, some of these molecules may be missing, thus leading to the failure in B cell activation and antibody production.

      Anne S

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