Autoimmune markers in lymphoid malignancies

Chronic immune stimulation such as Helicobacter pylori (hp) infection, Sjögren's syndrome or coeliac disease may initiate non-Hodgkin lymphoma (NHL). The opposite (appearance of autoimmunity) has also been reported. The aim of this study was to describe the pattern of these immune markers in patients with lymphoid malignancies. Sera from 96 patients with NHL (median age 72, range 38-88, F/M 41/55) were analysed with ELISA to determine the frequency of antibodies against guinea pig (gp) and human recombinant (hr) transglutaminase type 2 (Tg2), and hr factor XIII subunit a* (part of the Tg-family), extractable nuclear antigen (ENA), and hp. As hp antibodies decrease in younger age cohorts a sex- and age-matched control group of 768 persons was used. The control population for transglutaminase antibodies consisted of 59 blood donors, (median 42 years, range 19-65) was analysed with a commercial kit. Gp-Tg2-IgG positivity was documented in 72% and hr-Tg2-IgG positivity in 15% (5% positive controls for both; P < 0.001 and ns, respectively). For IgA 3% had gp-Tg2 and 4% hr-Tg2 (5% in controls: ns for both). Anti-FXIII-IgA positivity was found in 22% (5% in controls; P = 0.03). Unspecific anti-ENA-IgG positivity was found in 24% (P < 0.001), while only 2% had specific ENA autoantibodies. Moreover, 36% were positive for anti-hp-IgG, while controls were positive in 54% (P < 0.001). The frequency of unspecific autoantibodies was increased. No differences could be noted in specific autoantibodies (hr-Tg2-IgA). In contrast, fewer than expected were anti-hp-positive. A defective immune response, similar to that in autoimmune diseases, could contribute to the pathogenesis of lymphoid malignancies.