Do infections boost the climb of our B-lymphocytes?

Given our bodies can respond to infections by boosting our lymphocyte count, has anyone noticed a permanent step up in their lymphocyte counts following infections? (I'm wondering if there is a correlation between frequent infections and a more rapid increase in the lymphocyte count? It was found out recently that malignant lymphocytes do die off in CLL patients, but they are more than replaced by new ones. Perhaps the die off rate changes post infection too...)

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  • Hi Neil...good question...

    The work of Nicholas Chiorazzi and the Heavy water study turned our understanding of cell proliferation in CLL on its head... in regards to antigen response proliferation this paper has a good discussion in section B2, but I recommend complete read...

    asheducationbook.hematology...

    ~chris

  • Here is briief article about Chiorazzi's heavy water study...see page 2 of this PDF...

  • Sorry here is the link..

    feinsteininstitute.org/cs/S...

  • Thanks Chris,

    So in summary, going by all the theorising in this very interesting, ground breaking paper, we still have so much more to learn. If I read it correctly, for some of us, depending on our mutation status and particular mutant clone, infections could well be a significant driver, in particular for those with unmutated status - which would also somewhat explain the generally poorer prognosis for those with that status...

    Another good reason to avoid infection if at all possible!

  • Hi Neil Interesting question

    There are two CLEAR trials in the UK studying early CLL one for those with good and one for poor prognostic markers I think they are studying the mechanisms connected with bacterial infection that may drive the development of early CLL. This data should be very interesting and identify differences between different sets of prognostics..

    Chris, there are so many articles about this now to read when you Google the library. It is very complicated and confusing so many things seem to be going on. So many questions.

    Does immune response and the pro-inflammatory state alter counts by increasing turnover and by preventing some cell death? Does residua/chronic infection maintain or drive these immunity/inflammatory responses?,Do proliferation micro environments continue to sustain this? Does the tumour cell itself aid all this by it's own cytokine secretions? Does increased cell turnover raise the chance of creating clones more prone to survival that are able to develop their inflammatory microenviroment, and encourage further proliferation and protection from nurse cells? I have read several interesting recent papers by Federico Caligaris-Cappio and team in this area .

    I guess you are right trying to remain infection free and controlling inflammatory conditions makes sense..

    Reading posts from people and observing my own PB lymphocyte counts while they were rising they did in steps on the graph but I couldn't correlate these to any specific infection or condition. other than when an infection was cleared counts improved a little.

    Interesting stuff heavy water., was only talking about it recently and it's use in a UK trial to study T cell proliferation and involvement with CLL progression.

    Nick

    PS on a positive note:my blood counts have steadily improved for 8 months following a heart intervention that has improved a chronic inflammatory condition. ?

  • Very astute questions Nick! I'd thought along similar lines after reading the paper Chris referenced but hadn't thought it through in any where as much detail. So many avenues ripe for investigation!! Be great if we could uncover some easily implemented strategies like improved infection prevention and more attention to reducing chronic inflammation conditions. Could give some valuable breathing space while we wait for better treatments than FCR to be approved.

    Neil

  • Interesting Nick...when I lost all my weight...my absolute lymphocyte count (ALC) dropped slowly over 18 months from 132K to 42K. The general view of my team is my excess baggage had ramped up the immune system for years and created a chronic inflammation condition, that pumped up the volume on the B lymphocytes. However, after a year at the 42K level...my absolute lymphocyte count (ALC) rocketed up to the old level with node involvement, which I never had before... so something definitely changed. Regrettably FISH aren't done here, but my feeling is I likely changed from a single to a mixed karyotype...this would explain a more aggressive driver after 13 years of very indolent CLL.

    I'm writing this from the infusion room...currently having cyclophosphamide and then rituxan... last round of R-CEP!!

  • Chris, thanks for posting and sharing this how much longer in the chair?

    FISH is not done here routinely pre-treatment unless there are physical concerns. But it is important at treatment to identify refractory disease.

    I wonder what could have suddenly triggered the drive. a change in the equilibrium? A more progressive clone created in the freed up space allowing progression or it was there but had been kept at bay by numbers and was then able to proliferate? A liquid disease with a solid tissue problem. Good reason to have one eye still over my shoulder (- :

    I forgot to mention my weight loss and diet change for good heart health that accompanied the rehabilitation following the intervention. Net result is I also lost weight over this time period (could this be contributing?). I wish the arthritis was responding though (small potatoes) (-:

    Good luck

    PS just looked up R-CEP, because of neuropathy?

  • Not scientifically informed enough to add to this debate but get the drift and it poses interesting questions.

    Really wanted to say hope the treatment goes well for you Chris...such dedication writing this from the infusion room. I bet the longer treatment sessions get very boring and tedious at times! Hoping for 'success' for you.

    Newdawn

  • I think this is an absolutely crucial question.

    Vaccinations are intended to give your immune system a bit of a wake-up call, and adjuvants that increase the immune response are also sometimes recommended. What if this actually accelerates the progress of CLL? Don't you think there should be some effort to address this question?

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