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Rheumatology 2000; 39: 1060-1066
© 2000 British Society for Rheumatology

Review

HLA association with autoimmune disease: a failure to protect?

E. Zanelli, F. C. Breedveld1 and R. R. P. de Vries

Departments of Immunohaematology and Blood Bank and
1 Rheumatology, Leiden University Medical Centre, Leiden, The Netherlands

That certain HLA specificities are associated with predisposition to autoimmune disease does not necessarily imply that self-reactive T cells restricted to particular HLA alleles are eliciting the disease. In the present essay, we argue that HLA can be a major genetic factor in the development of autoimmune diseases without T cells being primarily involved in its initiation or perpetuation. There is now ample evidence that self-reactive, regulatory T cells can protect against pernicious autoimmunity. Hereafter, we propose that extended HLA haplotypes, such as DQ3-DR4, DQ3-DR9, DQ5-DR1 and DQ5-DR10 in the case of rheumatoid arthritis, predispose to impaired T-cell-mediated immune regulation. The haplotypes associated with impaired regulation are the combination of certain class II alleles and a yet unknown ‘amplifier’. In this model, products of the HLA class II region are not involved in the presentation of particular organ-specific autoantigens. Therefore, HLA does not predispose to autoimmune disease per se, but rather fails to provide efficient protection.

Correspondence to: E. H. Zanelli, Department of Immunohaematology and Blood Bank, Leiden University Medical Centre, Albinusdreef 2, Bldg. 1, E3-Q, PO Box 9600, 2300RC, Leiden, The Netherlands.


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