The number of DNP group-bearing lymphocytes in the regional lymph node, thoracic duct and peripheral blood was determined at various time intervals after painting normal guinea pigs with DNCB by the immunofluorescent method using anti-DNP antibody. The incidence of such cells in the regional node was maximal at 12 hours whereas in the thoracic duct and peripheral blood the maximum incidence was found at 0.1-2 hours after painting. Unreacted DNCB was demonstrated in both the thoracic lymph duct and the blood at least for 12 or 24 hours respectively following exposure to DNCB. The authors therefore suggest that DNCB reacts directly in vivo with the lymphocyte cell membrane of guinea pig following epicutaneous application of the chemical.

DNCB-sensitized guinea pigs demonstrated an accelerated reactivity on retest of DNCB at the site of prior contact reaction, though presenting normal contact sensitivity at the virgin site. The retest reaction reached maximal at 9 h and waned at 24 h after antigenic challenge. Massive accumulation of eosinophils in either the epidermis or dermis was its distinguishing histologic feature. The reaction was induced at the site of delayed skin reaction to DNP-GPE in the animals sensitized with DNCB or DNP-GPE. A retest reaction in delayed sensitivity to DNP-GPE was also elicited at the site of contact reaction to DNCB in the animals.

The incidence of dinitrophenylated cells in guinea pig lymphocytes incubated with 0–30 m_M concentrations of DNBSO₃Na in phosphate-buffered saline was examined by an immunofluorescence method using fluorescence-labelled anti-DNP antibody. Under our experimental conditions, the incidence was roughly proportional to the concentration used. Using DNP-lymphocytes as an antigen for skin testing, a marked delayed reaction was induced in guinea pigs sensitized by painting with DNCB and intradermal injection of Freund’s complete adjuvant. The significance of these findings is discussed.

In vivo deposits of fibrin, fibrinogen, plasminogen, complements and immunoglobulins were observed using immunofluorescent (IF) staining of psoriatic lesions. Deposits of fibrin were seen in either the horny layer or the dermal papillae. A linear cytoplasmic appearance of fluorescence in the psoriatic scales was a common pattern of the staining. "IFstaining of the psoriatic horny/layer for fibrinogen and plasminogen' yielded essentially the same pattern as those of fibrin and IgG.These findings suggest that some fibrinolytic processes may be associated with an immune reaction in psoriatic skin, although they be secondary phenomena.The autoimmune hypothesis concerning the etiopathology of psoriasis is largely based on the demonstration of serum autoantibody to stratum corneum and complement-mediated immune complexes in the superficial layers of the psoriatic epidermis. It has been shown by Krogh (1), Beutner et al. (2) and Jablonska et al. (3) that in psoriasis, as well as in healthy controls, circulating antibodies are present and reactive with the membrane of the horny layer cells. These antibodies are of complement binding type. The in vivo binding of either immunoglobulin or complement with horny layer cells has also been demonstrated in psoriatic lesions (2-5). Cormane et al. (6) have observed in addition the presence of various immunoglobulins in the nuclei of the parakeratotic cells. The deposits of various immunoglobulins and complements In psoriatic skin are also associated with the appearance of fibrin and fibrinogen (7-10).The objectives of the studies presented in this report were to demonstrate the association of a fibrinolytic process with the immune reaction in psoriatic skin. MATERIALS AND METHODS Case studiedEighteen cases, II males and 7 females, of common psoriasis with characteristic lesions and histologic changes were studied. The age of the patients ranged from 22 to 83 years, and the duration of the disease was from I to 14 years. Immunofluorescent (IF) methodsThe biopsied skin specimens were quick-frozen, cut on a cryostat, air-dried without fixation and incubated with either antisera or FITC-labeled conjugates for 30 minutes at room temperature. Antisera and FITC-labeled conjugates were absorbed twice with mouse liver acetone powders and diluted to suitable concentrations before incubation. The direct IF method was utilized for the detection of IgG, IgM, PIc, c, activator (CsA), Clq and fibrin, while the indirect method was used to detect plasminogen, fibrinogen and fibrin degradation product (FDP) in the skin using FITClabeled antirabbit y-globulin antibody. The FITClabeled conjugates were purchased from Medical and Biological laboratories LTC and antiplasminogen, fibrinogen and FDP sera from Dakopatts and Behringwerke AG. The F -P molar ratio of the conjugates ranged from 1.0 to I. 78 and antibody concentrations were between 30 and 50,ulml. Blocking tests were performed on the serial sections using unlabeled antisera and antigens.

A case of Schonlein-Henoch-purpura is presented. The immunofluorescent study of skin lesions of the patient showed granular deposits of IgA and C3 in the blood vessel walls perivascular deposits of plasminogen and diffuse localization of fibrin and fibrinogen in the upper dermis. Complement activation via the alternative pathway through IgA, C3 and plasminogen deposits was suggested.