The pregnant patient has Behcet's disease and also Rubella IgM positivity. False positive IgM results may appear because of B cell activation. Can Behcet's disease cause such a response?
It seems that there is a hypothesis that partly explain the etiology and pathogenesis of autoimmune disease called "molecular mimicry". It means foreign antigen from pathogens may cause antibody recognize their specific epitopes, if the sequence of the eptiopes are similar (sequence or physicochemical property) with the epitope of our own protein. the antibody arouse by pathogen may turn to attack our own protein and become autoantibodies, then cause an autoimmune disease.
So maybe here is the same situation. If the autoantigen of behcet's disease share a common epitope with the foreign protein from pathogen which cause rubella, the auto produced IgM could also recognized the rubella virus antigen, which cause the serologic test false positive.
Those are all a little opinion base on my own understanding.
it is not possible to verify if the hypothetical auto-antigens of Behcet Disease are mimicrin the Rubella antigens. However, fo the health of both mother and fetus, I suggest to perform a molecular analisys to find the RNA of Rubella in the maternal blood. To my knowledge, this is the only way to verify if there is an active infection.
I am really interested about this case, please let me know the results.
We have no reason to think Behcet's disease is in fact autoimmune. There is no evidence of autoantibody formation as far as I know, and no evidence of autoreactive T cells. The most significant clue to the aetiology is B51, which, as for B27 in ank spond, suggests some sort of threshold shift in cytotoxic or NK cell interactions. There is similarly no evidence for ank spond being autoimmune. There is also little or no evidence for the old molecular mimicry theory in human disease. It is frequently cited but probably should have been discarded fifty years ago.
So I think it would be entirely inappropriate to speculate about a relation between Behcet's and antibody titres here. I would stick to clinical facts. I am not aware of any published evidence on false positive IgM titres in Behcet's.
the HLA-B*51 carriers among Behcet Disease patients are from 20 to 60% depending on ethnicity. This is why being a B*51 is not included as a crietium for Behcet Diagnosis from the International Society for Behçet's Disease (ISBD). There are many reports on the possible trigger by several viruses,
Autoimmun Rev. 2015 Jul;14(7):609-15. doi: 10.1016/j.autrev.2015.02.009. Epub 2015 Mar 11. The role of infections in Behçet disease and neuro-Behçet syndrome.
Marta M, Santos E, Coutinho E, Silva AM, Correia J, Vasconcelos C, Giovannoni G.
and there is also an open debate about wether Behcet is autoimmune or autoinflammatory
I agree we do not have sure answers, Cristina, but the fact remains that we have no reason to think Behcet's is autoimmune (no evidence for a specific anti-self response) nor that precipitation of symptoms by viruses (and of course also by needles) involves 'mimicry'.
B51 is not present in all cases, indeed, but nor is DR4 in RA, or B27 for AS, or female gender for RA (and none come into diagnostic criteria of course) but they remain clues to a type of pathogenesis. The presence of B51 in some cases points us towards a process that is sensitive to MHC Class I interaction thresholds - which also points us away from autoimmunity if anything. DR4 and RF pointed us to using rituximab in RA, etc. Many of us were educated at a time when 'autoimmunity' was a sloppily used word but I see no reason to associate it with Behcet's now that we know more than we did in 1970.
This topic is so interesting that I would continue to talk about it for days!
Ok, no more mimicry, I was not even born in 1970!
I know that in all immune-related pathologies the HLA alleles are only predisposing, not causing.
So, what is your personal point of view about Behcet and its etiology or pathogenesis? Maybe you think about a NK deregulation? I don't believe that HLA-B*51 is so important in Behcet pathogenesis because it is a KIR ligand, all HLA-B Bw4 epitopes bind to KIR, and even some HLA-A alleles too.
Please let me know your opinion.
Do you plan to participate to the upcoming Congress on Behcet Disease in Matera (Italy)?
I would consider that your patient (with Behcet) has been in contact with rubella virus. I would then look for RNA rubella virus in her blood as suggested by Cristina.
If you want to speculate about pregnancy and autoimmune disorders, we know that pregnancy can activation B cells as you have pointed out and Niklas has advised.
If this lady has previous pregnancies, we also know that pregnancy can leave a long-term legacy of bi-directional cell trafficking of fetal cells in the mother and of maternal cells in her offspring for decades after birth. This long-term persistence of a small number of cells (or DNA) from a genetically disparate individual is referred to as microchimerism. This phenomenon may happen here.
We also know that Behcet 's disease may have a cross reaction with soem strains of Streptococcus sanguinis. The same phenomenon may happen with rubella. This would then be the first case.