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Sera from patients with autoimmune diseases do not have circulating IgA antibodies against tissue transglutaminase

Sera from patients with autoimmune diseases do not have circulating IgA antibodies against tissue transglutaminase
Sera from patients with autoimmune diseases do not have circulating IgA antibodies against tissue transglutaminase
After the identification of tissue transglutaminase (TGc) as the predominant endomysial autoantigen of coeliac disease and dermatitis herpetiformis, diagnostic ELISAs were produced. Sera from patients with a broad spectrum of autoimmune diseases or with nonautoimmune diseases involving enhanced apoptosis, cell lysis and/or putative secondary autoimmune processes showed false positive reactions in these assays, as detected by a number of investigators. Sera from 605 patients and controls were tested in a human TGcELISA including 304 patients with autoimmune and 122 with other diseases. Anti-gliadin and anti-endomysium antibodies were also determined in 70 patients chosen at random. Overall 49% of all autoimmune sera were false positive in the human TGc ELISA. The difference between the median titers of the autoimmune and the control sera was significant in every case except for the pemphigus vulgaris sera (bullous pemphigoid, p¼0.012;pemphigus vulgaris, p¼0.152; SLE, p¼0.0005; antiphospholipid syndrome, p¼0.0002; for each of the other groups po0.0001). Significant differences were also found in serum titers between controls and patients with hepatitis C (po0.0001), psoriatic arthritis (p¼0.0065),and malignancies (p¼0.0005). Altogether 25% of the sera from patients with hepatitis C, psoriatic arthritis, and malignancies were positive in the human TGc ELISA. In contrast, testing 70 of the false positive patients for total serum IgA levels, AGA and EMA reactivity as well as immunoblots showed that no association of these conditions with gluten sensitive enteropathy can be confirmed. However, further purification of the TGc protein preparation used for coating and elevation of ionic strength in the buffers could eliminate false positive signals.
The currently used method for TGc ELISA allows nonspecific positivity of certain sera from patients having circulating IgA of high affinity against impurities. Thus it is evident that positivity of a TGc ELISA should not alone be taken as the basis for a diagnosis of coeliac disease or dermatitis herpetiformis.
0022-202X
p.A66
Sardy, M.
e7725514-7ec2-4630-962d-2c0c3c148378
Csikos, M.
a1cf9a6d-c048-4f58-aacd-e727bd982cf3
Geisen, C.
e263dcbc-4c4f-4469-acd3-0df69f3f82b6
Preisz, K.
281414f4-a8d8-4978-bfbb-3d1dd84e55ff
Kornsee, Z.
b3215381-7f8a-469c-902b-f613e0d923ab
Tomsits, E.
06bce16f-4007-42f4-bcb2-7115d7335c76
Tox, U.
1cdc19e1-f4b3-4262-a129-57220e8d78e2
Wieslander, J.
280423a4-d5c8-454f-a16b-ecaf900c6980
Karpati, S.
5f8086b6-966c-4fb2-b820-80722cec7e0c
Paulsson, M.
ada2e3d2-51b9-4a51-b350-15ac7870dc48
Smyth, N.
0eba2a40-3b43-4d40-bb64-621bd7e9d505
Sardy, M.
e7725514-7ec2-4630-962d-2c0c3c148378
Csikos, M.
a1cf9a6d-c048-4f58-aacd-e727bd982cf3
Geisen, C.
e263dcbc-4c4f-4469-acd3-0df69f3f82b6
Preisz, K.
281414f4-a8d8-4978-bfbb-3d1dd84e55ff
Kornsee, Z.
b3215381-7f8a-469c-902b-f613e0d923ab
Tomsits, E.
06bce16f-4007-42f4-bcb2-7115d7335c76
Tox, U.
1cdc19e1-f4b3-4262-a129-57220e8d78e2
Wieslander, J.
280423a4-d5c8-454f-a16b-ecaf900c6980
Karpati, S.
5f8086b6-966c-4fb2-b820-80722cec7e0c
Paulsson, M.
ada2e3d2-51b9-4a51-b350-15ac7870dc48
Smyth, N.
0eba2a40-3b43-4d40-bb64-621bd7e9d505

Sardy, M., Csikos, M., Geisen, C., Preisz, K., Kornsee, Z., Tomsits, E., Tox, U., Wieslander, J., Karpati, S., Paulsson, M. and Smyth, N. (2004) Sera from patients with autoimmune diseases do not have circulating IgA antibodies against tissue transglutaminase. Journal of Investigative Dermatology, 123, p.A66. (doi:10.1111/j.1523-1747.2004.23244.x).

Record type: Article

Abstract

After the identification of tissue transglutaminase (TGc) as the predominant endomysial autoantigen of coeliac disease and dermatitis herpetiformis, diagnostic ELISAs were produced. Sera from patients with a broad spectrum of autoimmune diseases or with nonautoimmune diseases involving enhanced apoptosis, cell lysis and/or putative secondary autoimmune processes showed false positive reactions in these assays, as detected by a number of investigators. Sera from 605 patients and controls were tested in a human TGcELISA including 304 patients with autoimmune and 122 with other diseases. Anti-gliadin and anti-endomysium antibodies were also determined in 70 patients chosen at random. Overall 49% of all autoimmune sera were false positive in the human TGc ELISA. The difference between the median titers of the autoimmune and the control sera was significant in every case except for the pemphigus vulgaris sera (bullous pemphigoid, p¼0.012;pemphigus vulgaris, p¼0.152; SLE, p¼0.0005; antiphospholipid syndrome, p¼0.0002; for each of the other groups po0.0001). Significant differences were also found in serum titers between controls and patients with hepatitis C (po0.0001), psoriatic arthritis (p¼0.0065),and malignancies (p¼0.0005). Altogether 25% of the sera from patients with hepatitis C, psoriatic arthritis, and malignancies were positive in the human TGc ELISA. In contrast, testing 70 of the false positive patients for total serum IgA levels, AGA and EMA reactivity as well as immunoblots showed that no association of these conditions with gluten sensitive enteropathy can be confirmed. However, further purification of the TGc protein preparation used for coating and elevation of ionic strength in the buffers could eliminate false positive signals.
The currently used method for TGc ELISA allows nonspecific positivity of certain sera from patients having circulating IgA of high affinity against impurities. Thus it is evident that positivity of a TGc ELISA should not alone be taken as the basis for a diagnosis of coeliac disease or dermatitis herpetiformis.

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Published date: August 2004

Identifiers

Local EPrints ID: 56406
URI: http://eprints.soton.ac.uk/id/eprint/56406
ISSN: 0022-202X
PURE UUID: cd4cbd55-f9db-4795-8c42-1462ab2d336f

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Date deposited: 11 Aug 2008
Last modified: 22 Jul 2022 21:07

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Contributors

Author: M. Sardy
Author: M. Csikos
Author: C. Geisen
Author: K. Preisz
Author: Z. Kornsee
Author: E. Tomsits
Author: U. Tox
Author: J. Wieslander
Author: S. Karpati
Author: M. Paulsson
Author: N. Smyth

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