[color=blue][size=14] It is easy to make claims such as that, but difficult to prove any authenticity to such claims. Please provide a link for these "recent studies" you claim to have knowledge of. I have not seen any data from any recent studies claiming this "longer-term use being detrimental to the patients' immune system".
I was able to find the second study that you claimed I was making up.
Tysabri is causing an increase in B immune cells and in the long run, that is not good. Like I have said many times, there is a lot unknown about this drug and I fear that its long term use may cause some real problems.
BTW, I should be asking you for the same level of respect that you have demanded from Ursula. Stating that my statements are wrong when in fact they were not and inferring that I am making up information about clinical trials isn't exactly what I would call respectful comments. I have no problem with people disagreeing with my opinions. But I'm not too keen to have people infer that I am not being truthful.
Natalizumab disproportionately increases circulating pre-B and B cells in multiple sclerosis.
Krumbholz M, Meinl I, Kümpfel T, Hohlfeld R, Meinl E.
Institute of Clinical Neuroimmunology, Ludwig Maximilians University, Munich, Germany.
BACKGROUND: Natalizumab, a humanized anti-alpha4 integrin monoclonal antibody, reduces relapses and disease progression in patients with multiple sclerosis (MS). Whereas its presumed mode of action is inhibition of T cell/monocyte entry into the brain, little is known about its specific effect on B cells, which are increasingly recognized to participate in MS pathogenesis. METHODS: We obtained serial blood samples from 17 patients before and during natalizumab therapy for relapsing-remitting MS for up to 16 months, and blood samples from 10 untreated patients with MS and 13 healthy donors. We determined numbers of mature and immature lymphocyte subsets by flow cytometry for CD3, CD4, CD8, CD19, CD138, and CD10 in 111 samples. We analyzed marker transcripts for immature hematopoietic cells by quantitative PCR for CD34, Vprebeta1 (pre-B lymphocyte gene 1), and DNTT (terminal deoxynucleotidyltransferase) in 65 samples. RESULTS: Natalizumab therapy increased CD19(+) mature B cells more than other lymphocytes/monocytes in blood (2.8-fold versus 1.3-1.8-fold increase in cells/microL; p < 0.01). Even greater was the increase of immature CD19(+)CD10(+) pre-B cells (7.4-fold; p < 0.01). This pattern remained stable during treatment for up to 16 months. Transcripts of lymphocyte precursors (Vprebeta1 and DNTT) were elevated more than transcripts for CD34. CONCLUSIONS: Circulating B cells and especially pre-B cells are most prominently elevated among the studied immune cell subsets, raising the possibility that the effects and side effects of natalizumab are partly mediated by actions on B cells.