Learning from other conditions is useful. As there are more people with rheumatoid arthritis than MS we will see alot of anti-CD20 papers with rituximab. There will be subtle differences compared to ocrelizumab. So when you read the paper that says the vaccine response to anti-CD20 is unknown….it’s not its getting less unknown by the day. If you are taking ocrelizumab you should expect to be making protective T cells even whne you antibody response is inhibited
Mrak D et al. SARS-CoV-2 vaccination in rituximab-treated patients: B cells promote humoral immune responses in the presence of T-cell-mediated immunity.Ann Rheum Dis. 2021 Jul : annrheumdis-2021-220781.Published online 2021 Jul 19. doi: 10.1136/annrheumdis-2021-220781PMCID: PMC8295012PMID: 34285048
Objectives: Evidence suggests that B cell-depleting therapy with rituximab (RTX) affects humoral immune response after vaccination. It remains unclear whether RTX-treated patients can develop a humoral and T-cell-mediated immune response against SARS-CoV-2 after immunisation.
Methods: Patients under RTX treatment (n=74) were vaccinated twice with either mRNA-1273 (Moderna) or BNT162b2 (Pfizer). Antibodies were quantified using the Elecsys Anti-SARS-CoV-2 S (Roche) immunoassay against the receptor-binding domain (RBD) of the spike protein and neutralisation tests. SARS-CoV-2-specific T-cell responses were quantified by IFN-γ enzyme-linked immunosorbent spot assays. Prepandemic healthy individuals (n=5), as well as healthy individuals (n=10) vaccinated with BNT162b2, served as controls.
Results: All healthy controls developed antibodies against the SARS-CoV-2 RBD of the spike protein, but only 39% of the patients under RTX treatment seroconverted. Antibodies against SARS-CoV-2 RBD significantly correlated with neutralising antibodies (τ=0.74, p<0.001). Patients without detectable CD19+ peripheral B cells (n=36) did not develop specific antibodies, except for one patient. Circulating B cells correlated with the levels of antibodies (τ=0.4, p<0.001). However, even patients with a low number of B cells (<1%) mounted detectable SARS-CoV-2-specific antibody responses. SARS-CoV-2-specific T cells were detected in 58% of the patients, independent of a humoral immune response.
Conclusions: The data suggest that vaccination can induce SARS-CoV-2-specific antibodies in RTX-treated patients, once peripheral B cells at least partially repopulate. Moreover, SARS-CoV-2-specific T cells that evolved in more than half of the vaccinated patients may exert protective effects independent of humoral immune responses.
(A) Get vaccinated make an antibody response, (B) have B cells make an antibody response, (C&D) the more B cells the more likely you have an antibody response….(D) there are a few exceptions. Here have 3% B cells compared to lymphocytes and you make some form of an antibody response.
Most people also make a T cell response
Yes you are getting fed up seeing the same result over an over again. However it will be that you eventuallly believe this. Most neurologists are not looking at the arthrtitis literature and so it will take longer for the MS data to emerge….but emerge it eventually will.
So the water torture, drip drip drip is for them. So I am giving you MDs crystal ball to allow you to look into the fututre. Now I must say the kinetics may be different as the B cells will return slower with ocrelizumab than rituximab and so it will be harder to see. Most but not all people make anti-T cell response just like healthy people.
The big question is going to be will we try to exploit this information when boosters come or say thanks very much its good to know. I suspect the latter.
However if we plough on we should test to see what may happen when we boost before it it is nationally rolled out.
Would you prefer to be optimized to give the best response you can?
COI: multiple but not relevant
Disclaimer: Please note that the opinions expressed here are those of the author and do not reflect the positions of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust or Queen Mary Univeristy of London.