AbstractInfection with beta‐haemolytic streptococci is accepted as one of the triggering factors leading to exacerbation of psoriasis. In a long‐term study lasting nine years (1982–1991) we investigated whether there is any evidence of dysfunction of humoral and cellular immune factors, and what part is played by microbial infection in this connection, with specific reference to streptococcal antigens. 110 patients with chronic psoriasis, either clinically inactive (stage 1) or active with eruptions (stage 2) and 70 healthy controls underwent the following immunologic investigations: streptococcal antibody titres, serum immunoglobulins IgM, IgA, IgG, total serum IgE, complement factors C3, C4, B and T cells, and subpopulations. The findings demonstrate that phases of inactivity are associated with a mechanism described as “Immunologic Regulation”‐activated antibacterial titres and unremarkable findings for humoral and cellular parameters. Eruptions of psoriasis are with phases of humoral and cellular deficiency; antibacterial titres are significantly elevated, serum IgM or IgA or IgG show deficient levels, C3 is activated, C4 is decreased, as are serum IgE and T4:T8 ratio. Shift in T‐cell subpopulations may depend on serum IgE concentration.The question for consideration is whether antigen‐eliminating inflammatory lesions present in immunodeficiency phases trigger the formation of circulating immune complexes. It seems probable that the pathogenicity of these immune complexes is controlled by serum factors and that they are involved in the initiation of keratinocyte hyp