| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Letters |
1 Department of Clinical Sciences, University of Rome "La Sapienza", 155-00161 Rome, Italy
aAddress correspondence to this author at: Department of Clinical Sciences, Policlinico "Umberto I", University of Rome "La Sapienza", Viale del Policlinico, 155-00161 Rome, Italy. Fax 39-06-49970524; e-mail a.picarelli{at}flashnet.it.
To the Editor:
We read with interest the report (1) on IgG antibodies against tissue transglutaminase (tTG) in patients positive for anti-double-stranded DNA with systemic lupus erythematosus and in patients positive for anti-SSA/SSB. We agree with the authors’ hypothesis that in some autoimmune disorders, such as systemic lupus erythematosus, the content of apoptotic bodies (including tTG) could come into contact with the immune system, leading to an autoimmune response. Nevertheless, some aspects of this study require comments.
tTG, an intracellular enzyme, has recently been proposed as the major autoantigen of anti-endomysial antibodies (EMAs), and measurements of IgA anti-tTG antibodies are used in the diagnostic evaluation of celiac disease (CD) (2)(3)(4). Furthermore, the presence of IgG anti-tTG antibodies has been associated with IgG1 EMA positivity in CD patients either with or without selective IgA deficiency (5)(6). To exclude CD, we believe that determination of serum IgG1 EMA could be useful in the above-mentioned antinuclear-positive patients (1).
We have recently demonstrated that, in the occurrence of CD, tTG is released by fibroblasts into the extracellular matrix compartment (7). We also found IgA anti-tTG antibodies in EMA-negative patients with Crohn disease and ulcerative colitis, suggesting that anti-tTG induction could be attributable to tTG released into the extracellular matrix of tissue lesions rather than to the autoimmune component of CD (7). In support of this thesis, another study demonstrated the presence of IgA anti-tTG antibodies in EMA-negative patients with non-Hodgkin lymphoma (8).
These observations, together with the interesting data in the report by van der Sluijs and Vermes (1), lead us to hypothesize that tTG is not the only antigen for EMAs and that further studies are necessary to clarify the issue.
References
2 Department of Clinical Chemistry, Medisch Spectrum, TwenteHospital Group, Enschede, The Netherlands
bAuthor for correspondence. Fax 31-53-487-3075; e-mail labmst{at}euronet.nl.
To the Editor:
In the report cited above, we examined the diagnosis of celiac disease in our patients (none of whom had an IgA deficiency) by determination of IgA anti-gliadin and IgA anti-tissue transglutaminase (tTG). Drs. Di Tola et al. indicate that IgG1 anti-endomysial antibody determinations can also be useful for this purpose, which would support their theory that transglutaminase is not the only an-tigen of the endomysial antibodies. Another possible explanation of their findings concerns the nature of the antigen used in the anti-tTG assays. Our results in autoimmune patients could be found only with guinea pig liver tTG as the antigen in the assay. With recombinant tTG, at least the one prepared in a baculovirus system, the positivity of the anti-DNA and SSA/SSB samples for IgG anti-tTG disappeared (whereas the IgA anti-tTG in the celiac disease patients remained intact). From this finding (unpublished data), we concluded that the in vivo antigen from the apoptotic bodies differs from the "pure" tTG. This can be the result of different posttranslational changes in the tTG molecule or of neoantigens that occur only in tTG substrate complexes. Thus, in discussions about positivity of anti-tTG assays, the nature of the antigen used should always be specified. This holds as well for the antigen released in vivo, e.g., by fibroblasts.
It is a question of semantics, then, to state that tTG is not the only antigen of the endomysial antibodies.
The following articles in journals at HighWire Press have cited this article:
|
|
 |
|
  D. Villalta, N. Bizzaro, E. Tonutti, and R. Tozzoli IgG Anti-Transglutaminase Autoantibodies in Systemic Lupus Erythematosus and Sjogren Syndrome Clin. Chem., July 1, 2002; 48(7): 1133 - 1133. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
