From Dr Tamar Tadmor, Head of the Israeli CLL study group at iwCLL.
Patients with CLL suffer from varying degrees of immune deficiency, either due to their treatment or due to the the primary disease
These include:
1. functional defects of B and T lymphocytes, NK cells, neutrophils and macrophages,
2. hypogammaglobulinemia in “treatment –naïve” patients which develops even more frequently following therapy for CLL.
A positive antibody response to the vaccine was evident in only 160 (43%) of all patients with CLL. For the treatment naïve cohort: 61% responded to the vaccine and in the treated cohort: an inverse correlation was found between number of lines of prior anti CLL therapy and the development of a serologic response.
There was a serologic response in 23% of the BTKi patients and a statistical difference between patients receiving ongoing BTKi (18%) compared to previously treated patients (37%).
The T-cell response to the vaccine was determined by Interferon gamma (IFNγ) secretion in 83 patients in Israel with CLL following BNT162b mRNA Covid19 Vaccine.
Blood samples were stimulated ex-vivo with Spike protein and secreted IFNγ was quantified. 83 patients (68 were eligible for the analysis (with positive internal control)) at 3 medical centres in Israel
The results showed that a T cell immune response to the vaccine was evident in 22 (32%) patients.
**IMPORTANTLY and perhaps disappointingly** - There is a correlation between T-cell response and serologic response to the vaccine.
Jackie
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First thing for me is where do I sit, as a treatment naive Astra Zeneca recipient. Then theres the issue that had a pfeizer i am 61% probable to have raised antibodies. I recall an earlier study (I think the Birnmingham one) which specified that those who did have responses experienced much lower antibody levels than 'normal' people. Then the factor of if the vaccine fails how might we fare? More questions than answers it seems. I think on a personal level I'll take my third/ booster and will relax more when the numbers locally are lower and always be cautious but get on with things. I am concerned these figures will start to be ommitted from gov sites as we transition 'out of the pandemic', which of course we aren't in a global or medical sense, but in a social sense we are.
My understanding is that AZ produces a longer lasting effect.It’s a very strange situation we are in as everyone has flu jabs each year knowing they are at best around 50% effective (probably less in those immunocompromised) and there’s an underlying mortality of around 50K - 60K each flu season - around 400/day during the actual flu season - and no one is particularly bothered, it’s certainly not newsworthy.....
I’m not saying ‘don’t be cautious’.....more, there’s always going to be these risks - and we’ve lived with bigger risks year after year......all we can do is get jabbed and hope all the other >16 year olds see the bigger picture as well.......
Perfectly put, and I agree. We all need to do our own risk benefit analysis and for me I've come to terms that most likely it will be an infection which sees me off due to the CLL but hopefully not for a few years yet as I Am early in my journey and still 'young' (56) so I need a holiday and I need bike trips. I will knuckle down this winter I suspect and hopefully things will be better soon after. I say that in the knowledge that we would all be home in a boat by now but for delta.
Definitely will get one. Need to hope it is effective, there is significant infection of double vaxed with delta variant and I'm disappointed there are no 'tweaked' vaccines being suggested, tagetting variants more effectively.
I'm not at all sure I will be offered a 3rd jab since GPS have to refer for them and mine doesn't believe CLL is a proper cancer(he actually said that!) and didn't refer me to be on the shielded list until prompted by consultant.. We shall see no doubt
Whether it's a third or a booster, unless you're less than 50, you will be offered one. My understanding is they are the same, ie the original formula, though its likely/ possible you'll get a different 'brand' whether by luck or design I can't say. Generally there seems to be a lot of bluster in the press that this and that is going to happen by whenever and then it goes quiet. A few on here have reported getting an additional recent shot. I know one is NHS, not sure the other.
It certainly would be good to know I do my tests by post so I don't actually have face to face contact.. Do let me know what your discussion outcome is
OK, so after two vaccinations I have no antibodies. Had a third Pfizer jab and a blood test to measure for antibodies again 13 days later and I'll know the results next week. Consultant talking about a 4th jab if I still have no antibodies and I'm willing to try but I was very poorly after my 3rd jab for 3 days.In all honesty, I'm very fed up of limiting my social activity now that everyone else is living life pretty much to the full again. I'd be willing to try most things to be able to have some antibodies.
Are you on anti CD 20s my gp and hematologist put heads together and contacted vaccine committee to ask for a 4th and they said no for now I'll be v interested to hear what they say for you
That sounds hopeful.... I had Obinutumazab til end of June and evidently that leaves you unable to produce antibodies to any extent for a year after its finished
Thanks Jackie, can you please post a link ASA available. This study seems to expand on findings of an earlier study with fewer CLL patients, somewhat similar outcome though
The T cell response or lack there of is not surprising to me. As Dr Koffman once said about antibody producing B cells and our T cells, “They dance together. “
Thanks. Will this data be published for public consumption? It’s hard to get a good picture from some slides and snippets from the presentation. I get the overall gist of the study, but it’s always nice to have the complete presentation in hand.
Thanks. Not surprising. I know it will be disappointing to some, but it is better to know where you stand than act as if you have some type of protection, when you don't. I made mention of this in a post last December that rankled some. It makes complete sense if you can't generate antibodies, T cells won't be generated either, seeing as they are collaborators.
Keep your mask on and hope for a long lasting treatment like the antibody therapy they are currently working on. I think at Vanderbilt.
Yes! AZD7442! Apparently it failed as a treatment (Storm Chaser trial) but had excellent results as a prophylactic. I think this is the best development upon which to base our hopes for the long run. AZ is apparently soon to submit for FDA approval for long term (protection expected to last about a year following a single injection) prophylactic use based on the positive outcome of the Phase 3 Provent trial which showed that 77% of trial participants did not develop COVID compared to those taking placebo. Of those receiving AZD7442 who did develop COVID, there were no cases of severe disease or death. It is noteworthy that 25% of the cohort receiving AZD7442 (866 people) had comorbidities including compromised immune systems.
Most of the papers I've seen have focused on CD4+ helper T-cell response, which is important for activating B-cells to eventually create antibodies. Since many of use have hypogammaglobulinemia or impaired antibody response, the CD4+ results are not so interesting, I think.
What I'd like to see is more info on CD8+ cytotoxic T-cells, which is more important to CLL patients if we have poor antibody response or poor CD4 response. Cytotoxic T-cells can attack the virus by themslves. Here's one good article:
CD8+ T cells contribute to survival in patients with COVID-19 and hematologic cancer
Published: 20 May 2021
This paper is based on the COPE study (COVID-19 Outcomes in Patients with Cancer), and is based on a small subset of patients (n=77), with only 22 with hematological cancer. I think it's been posted elsewhere on HU.
"Thus, CD8 T cells likely play an important role in the setting of quantitative and qualitative B cell dysfunction in patients with lymphoma, multiple myeloma and leukemia undergoing αCD20 therapy, chemotherapy or Bruton tyrosine kinase inhibition. Indeed, we could identify SARS-COV-2-specific T cell responses in most patients with hematologic cancer, including all patients treated with αCD20, and they were generally greater in magnitude than in patients with solid cancer. These SARS-CoV-2-specific T cell responses correlated with peripheral activated CD8 T cells, but not CD4 T cells, in patients who recovered from infection. These data suggest a role for SARS-CoV-2-specific CD8 T cells in controlling acute infection, although more definitive studies are needed. These observations also have important translational implications. CD8 T cell counts might inform on the need for closer monitoring and a lower threshold for hospitalization in patients with COVID-19 and hematologic malignancy. Furthermore, the clinical benefit of dexamethasone, which demonstrated an overall mortality benefit in hospitalized patients with COVID-19, but is known to suppress CD8 T cell responses[58], should be investigated further in patients who recently received αCD20 therapy."
Extended Data Fig. 8: Effect of cancer treatment on T cell differentiation in COVID-19.
It graphically shows the CD4 and CD8 T-cell and CD19 responses vs. type of therapy.
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One of the problems we face is that there is not yet a quantitative CD8 T-cell test commonly available for SARS-CoV-2. In the U.S., there is the T-Detect test from Adaptive Biotechnologies, which I believe the LLS is also using in their vaccine study. But it's qualitative - T-cell response detected vs undetected - and does not distinguish between CD4+ and CD8+ response. This is the frontier of SARS-CoV-2 immunological testing.
I don't want to minimize the importance of CD4 cells. They have a variety of functions. They do help stimulate CD8 T-cells, too. But I suspect that CD8 response is the thing we want to see measured the most.
In sum, I want to give those of us in therapy some hope that this hidden part of their immune system is still active, and is indeed helping. It may not fully protect us from infection, hospitalization, or death, but we're not entirely helpless. Antibodies are not our only defense.
Additionally, researchers rarely take into account the nutritional status of patients, since the study design doesn't allow it. Unfortunately, many people (chronic disease or not) eat poorly if they are choosing a standard Western diet with lots of processed & junky foods. I am confident that the many of us here, who are on the "I eat enough protein, get my micronutrients, and avoid an excessively inflammatory" diet, are the ones getting the good results. You can't make optimum antibodies even if considered "healthy" without ingesting enough of the necessary building blocks.
IDK of any large ones done in cancer patients, only diabetic and cardiac ones. I once worked with a practice group treating Cystic Fibrosis kids, and it was here I learned the "optimum nutrition" term. Kids who followed "optimal nutrition" had a lessened disease severity. Then when hemoglobin A1C was discovered, and how people who had elevated levels were encouraged to modify their diet & exercise to prevent diabetes development, and it worked, made me more of a "believer".
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Longitudinal analysis shows durable and broad immune memory after SARS-CoV-2 infection with persisting antibody responses and memory B and T
