Decreased B and T lymphocyte attenuator in Behcet’s disease may trigger abnormal Th17 and Th1 immune responses

Behcet's disease (BD) is a mysterious multisystemic disorder characterized by recurrent involvement of mucocutaneous (including recurrent aphthous stomatitis; RAS), ocular, intestinal, vascular, and/or nervous system organs. Previously, the positivity of “pathergy test”, which is one of the diagnostic examinations, was reported to be related to the possession of HLA-B51 gene in BD patients, even though the positivity is low and different from the countries. Here, instead of the ordinal pathergy test, we would like to propose the prick with self-saliva as a new diagnostic way for patients with RAS of BD based on the genetic intrinsic factors including HLA-B51 and extrinsic triggering factors. BD patients are considered to acquire the hypersensitivity against oral streptococci through the innate immune mechanism in the oral cavity. Bes-1 gene and 65 kD of heat shock protein (HSP-65) derived from oral S. sanguinis are supposed to play important roles as extrinsic factors in BD pathogenesis. Although the prick positivity was not related to the possession of HLA-B51 gene, the method is suggested to be a significant way for BD diagnosis. The results also suggest that BD symptoms are due to the vascular immune responses by monocytes expressed oral streptococcal agents of the patients.

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Oral Health and Its Aetiological Role in Behçet's Disease

Frontiers in Medicine ◽

10.3389/fmed.2021.613419 ◽

2021 ◽

Vol 8 ◽

Author(s):

Gonca Mumcu ◽

Farida Fortune

Keyword(s):

Oral Health ◽

Immune Responses ◽

Behçet’S Disease ◽

Behcet’S Disease ◽

Behçet's Disease ◽

Oral Microbiome ◽

Cutaneous Manifestations ◽

Behcet's Disease ◽

Oral Ulcers ◽

Complex Interactions

Behçet's disease (BD) is a chronic multi-systemic inflammatory disorder characterised by oro-genital ulcers, cutaneous manifestations, ocular, vascular, neurologic and gastrointestinal involvement. Complex interactions operating on the genetic background e.g.(HLA51), of infectious and other environmental agents, together with immune dysregulation impacts on the pathogenesis of BD. This suggests that the environmental factors triggering immune responses may activate clinical manifestations in genetically susceptible individuals. Since oral health forms the basis of all general health both dental and systemic, it is an important component of both Dentistry and Medicine. Oral ulcers are the most common clinical manifestation of oral mucosal health. Changes in the oral environment consequently acts as an infective and immune trigger. In this review, complex interactions between the oral ulcers, the oral microbiome and immune responses together with the course of oral and systemic disease manifestations in BD are discussed in the context of the aetiologic role of oral health.

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HLA antigens associated with Behcet's disease

Archives of Dermatology ◽

10.1001/archderm.113.12.1720 ◽

1977 ◽

Vol 113 (12) ◽

pp. 1720-1721 ◽

Cited By ~ 4

Author(s):

F. Ersoy

Keyword(s):

Behçet’S Disease ◽

Behcet’S Disease ◽

Behçet's Disease ◽

Hla Antigens ◽

Behcet's Disease

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Coagulation and Fibrinolytic Activity in Behçet's Disease

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646409 ◽

1991 ◽

Vol 66 (03) ◽

pp. 292-294 ◽

Cited By ~ 57

Author(s):

K K Hampton ◽

M A Chamberlain ◽

D K Menon ◽

J A Davies

Keyword(s):

Plasminogen Activator ◽

Tissue Plasminogen Activator ◽

Behçet’S Disease ◽

Fibrinolytic Activity ◽

Behcet’S Disease ◽

Behçet's Disease ◽

Plasminogen Activator Inhibitor ◽

Behcet's Disease ◽

Tissue Plasminogen ◽

Von Willebrand

SummaryCoagulation and fibrinolytic activities were studied in 18 subjects with Behçet's disease and compared with results from 14 matched control patients suffering from sero-negative arthritis. Significantly higher plasma concentrations (median and range) were found in Behçet's patients for the following variables: fibrinogen 3.7 (1.7-6.9) vs 3.0 (2.0-5.1) g/1, p <0.05; von Willebrand factor antigen, 115 (72-344) vs 74 (60-119)%, p <0.002; plasminogen activator activity (106/ECLT2) 219 (94-329) vs 137 (78-197) units, p <0.002; tissue plasminogen activator inhibitor (t-PA-I) activity, 9.1 (5.5-19.3) vs 5.1 (1.8-12.0) IU/ml, p <0.002; and PAI-1 antigen, 13.9 (4.5-20.9) vs 6.4 (2.4-11.1) ng/ml, p <0.002. Protein C antigen was significantly lower: 97 (70-183) vs 126 (96-220)%, p <0.02. No differences were observed in antithrombin III activity or antigen, factor VIII coagulant activity, fibrinopeptides A and Bβ15-42, plasminogen, α-2-antiplasmin, functional and immunological tissue-plasminogen activator, thrombin-antithrombin complexes and D-dimer. Levels of tissue plasminogen activator inhibitor (activity and antigen) correlated with disease activity while fibrinogen and von Willebrand factor concentrations did not. Seven of the 18 subjects with Behçet's disease had suffered thrombotic events but it was not possible to distinguish these from the 11 patients without thrombosis using the assays performed. The results suggest the abnormal fibrinolytic activity in Behçet's disease is due to increased inhibition of tissue plasminogen activator. No abnormality of coagulation or fibrinolytic activity specific to Behçet's disease was detected.

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