HLA-antigens in patients with allergic contact sensitivity to nickel.

Abstract

Associations between HLA antigens and certain diseases are well established [1]. Genetic control of contact sensitivity has been demonstrated in mice [2] and a relationship between skin sensitization to antigens and histocompatibility antigens was also described in guinea pigs [3]. Both in mice and guinea pigs T cell immune responsiveness, including delayed type hypersensitivity, has been found to be controlled by the major histocompatibility gene complex [4] In humans several investigations have been performed on HLA associations to contact sensitivity. One study demonstrated increased frequency of HLA-B8 in nickel allergy and o f HLA-B7 in multiple contact allergy among Northern Swedish subjects [5]. Another study showed that nickel sensitivity was positively associated with HLA-B21 [6] while a third report did not demonstrate any differences in HLA distribution between nickel sensitive females and controls [7]. These reports were all based upon typing for HLAA and B antigens only. However, several studies have demonstrated stronger associations to certain diseases of antigens of the H L A D / D R than the HLA-A and B series, particulary diseases where autoimmune mechanisms have been suspected. Secondly, as we have demonstrated previously, the H L A D / D R antigens of Langerhans cells play an instrumental role in the antigen presenting capacity of these cells [8]. We therefore performed typing both for HLA-A, B, C and DR antigens in 53 patients with contact allergic dermatitis to nickel, as determined with a positive epicutaneous patch test to nickel. The test was performed according to the European Standard Series with 5 % nickel sulphate in petrolatum, and read after 48, 72 and 96 h. All the patients reacted with erythematous infiltration and papules or vesicles. HLA-A, B, C and D R typing was performed as described earlier [9], using highly selected antisera, many of which have also been included in the International Histocompatibility Workshops. Some of the patients included in the study were also typed for HLA-D, using homozygous typing cells, as described earlier [10]. The HLA frequencies in the patient group was compared with the frequencies among healthy Norwegians. No significant associations to any HLA antigens were found. HLA-DR4 was found to be present in 42 % of the patients, versus 20 % in the healthy Norwegian population; and HLA-DR7 was present in 23 ~ of the patients versus 1 0 ~ in the population. These differences were, however, not significant when corrected for the number of antigens tested. Nineteen of the patients also reacted to cobolt. In this group the frequency of B8 was 5 % versus 25 5/00 in the normal population, DR4 was present in 47 % and DR7 in 32 %. None of the differences were significant when corrected for the number of antigens tested. We therefore conclude that in our study no associations between certain HLA antigens and nickel sensitivity was found.