IgG-Fc receptors in stratum granulosum: an immunological defence in human skin?

Receptors for the Fc-part of IgG (Fc tau R) in stratum granulosum of normal human skin were examined using cryosections and indirect immunofluorescence staining with 1) soluble immune complexes and 2) monoclonal antibodies (MoAbs) against different types of Fc tau R, i.e. 32.2 (anti-Fc tau I-CD64), IV.3 (anti-Fc tau RII-CD32) and Leu 11b (anti-Fc tau RIII-CD16). The immune complexes gave staining corresponding to stratum granulosum in sections from all skin specimens. Inhibition experiments showed that pre-incubation of the sections with monomeric and heat-aggregated human IgG, periodic acid and formaldehyde inhibited the immune complex binding. F(ab')2 containing immune complexes did not bind to the skin sections. The MoAb 32.2 gave granular and Leu 11b linear staining corresponding to stratum granulosum. In addition, both IC, 32.2 and Leu 11b gave weaker staining of keratinocytes in other parts of the epidermis. IV.3 stained epidermal Langerhans' cells and were unreactive with other epidermal cells. Indirect immunofluorescence staining with MoAbs against IgG subclasses showed the presence of all IgG subclasses in stratum granulosum. The results show that granulosum cells express both high- and low-affinity IgG receptors and in vivo bound IgG. The data point to a role for stratum granulosum in cutaneous immunity.

Fc gamma-receptors in skin and serum from patients with psoriasis, before and after therapy.

IgG-Fc receptors (FcR) are present on most immune competent cells. We have examined FcR in skin lesions from 8 patients with stationary plaque psoriasis and 12 patients with highly active psoriasis using MoAbs against FcR and binding of soluble immune complexes. FcR in serum were measured in ELISA. The patients were treated with cyclosporin (n = 5), acitretin (n = 7) and Goeckerman regimen (n = 8). As controls served 8 skin biopsies and 22 sera from healthy individuals. Highly active psoriatic lesions showed strongest activity for FcRI, II and III and immune complex binding. The FcR+ mononuclear cells were located perivascularly and along the dermo-epidermal junction. The FcR activity decreased in correlation to the improvement following therapy. Epidermal Langerhans cells (LC) were positive for FcRII and immune complex binding. FcR activity on LC decreased during therapy. Keratinocytes expressed FcRI and III, irrespective of disease activity and therapy. FcR levels were lower in sera from psoriatics than in controls, median 0.15 vs. 0.27 (p < 0.01), and not correlated to disease activity. In 4 patients the FcR levels increased during therapy. The reduced levels of FcR in psoriatic sera might be due to consumption in the skin or anti-FcR autoantibodies.

Serum levels of interferons and TNF-alpha are not correlated to psoriasis activity and therapy.

Sera from 52 patients with psoriasis and 106 controls were tested for IFN-tau, IFN-alpha 2 and TNF-alpha in ELISA and for total IFN activity using an infectivity inhibition micromethod. Psoriasis patients had lower serum levels of IFN-tau than had the controls: median 0.10 ng/ml vs. 0.16 ng/ml (p = 0.01). The highest median serum IFN-tau levels were in patients with peripherally spreading psoriasis, 0.10 ng/ml, and acute guttate psoriasis, 0.09 ng/ml. Patients with stable plaque psoriasis had lower serum IFN-tau levels (median 0.0) than those with other forms of psoriasis, or blood donors. The serum levels of IFN-alpha 2, total IFN activity and TNF-alpha did not differ between the psoriasis and control group. Treatment with cyclosporin, acitretin and the Goeckerman regimen increased the total IFN activity, but did not affect the levels of IFNs nor TNF-alpha.