Detection of arthritogenic factor in adjuvant arthritis.

An evocation of arthritis by an Ag-specific lymphokine has recently been considered with the description of arthritogenic factor (AF) in rats with collagen arthritis. Because rats with CFA-induced arthritis also exhibit T cell reactivity to native type II collagen, T cell lines specific for this protein were established from CFA-injected rats. Supernatant material from these lines contained a type II collagen-binding lymphokine with functional and biochemical attributes identical with those described for AF, i.e., it was a 65-kDa species cross-reacting immunoprotein possessing the ability to incite an erosive, proliferative synovitis when injected into the knee joint of naive recipients. Similarities were also observed with HPLC and on two-dimensional gels. Lymph node cells from rats with arthritis created by injection of the synthetic adjuvant, CP-20,961 failed to produce AF, suggesting that this material is not a ubiquitous concomitant of inflammatory arthritis in the rat. Test injections into sites contiguous with the ear cartilage plate and into fibroblast-lined s.c. pouches suggested that cartilage was a requisite for the induction of inflammation by AF. These data identify a potentially shared effector pathway in the collagen and adjuvant models. The presence of AF in two frequently used models further supports the hypothesis that Ag-specific lymphokines can create autoimmune disease.

Arthritogenic effects of Mycoplasma arthritidis T cell mitogen in rats.

The intraarticular injection of Mycoplasma arthritidis T cell mitogen (MAM) produced significant joint swelling with inflammation in DA rats. Histologic examination of the joint initially showed edema below the synovial surface layer with light polymorphonuclear and focal lymphoid cell infiltration. Widespread but incomplete shedding of the surface layer of the synovial membrane and hypertrophy and hyperplasia of the subsynovium with fibroblasts and macrophages were observed subsequently. The hyperplastic process began to resolve by Day 5 and almost completely disappeared by Day 7 with healing of the surface layer, leaving virtually no trace of the preceding acute episode. Arthritis in animals with previous adjuvant induced arthritis was not exacerbated by the intraarticular injection of MAM.

[High-dose intravenous penicillin therapy in neurosyphilis: study of 62 cases. II. Evaluation of cerebrospinal fluid]. / Penicilinoterapia intravenosa em altas doses na neurossífilis: Estudo de 62 casos. II. Avaliação do líqüido cefalorraqueano.

Sixty-two patients with symptomatic neurosyphilis were treated with 20 or 24 megaunits of intravenous penicillin G daily for 15 to 30 days. The mean follow-up time after the treatment was 30 months. Forty-one patients had pleocytosis in the CSF before treatment. Six months and twelve or more months later, abnormal cell count was observed in 4 (9.8%) and in 3 patients (7.3%), respectively. The CSF protein level and the titers of Wassermann reaction in the CSF decreased slowly after treatment. The gammaglobulin concentration of the CSF and the immunoglobulin production inside the blood-brain barrier were still increased beyond the first year after treatment. The results of the treatment of these patients with high doses of intravenous penicillin G were not different from the results verified with lesser doses of intramuscular penicillin that were reported in the literature.

Flow cytometric quantification of T6-positive cells in psoriatic epidermis after PUVA and methotrexate therapy.

We describe a flow cytometric technique for measuring the percentage of T6-positive cells in suspensions prepared by trypsinization of human epidermis. The value obtained for healthy controls (1.55 +/- 0.52%) corresponds to about 600 T6-positive cells per mm2 of skin surface, a figure in line with histological estimates. No significant change was found in the percentage of T6-positive cells in either the uninvolved or lesional epidermis of untreated psoriatic patients. PUVA treatment resulted in a significant reduction in T6-positive cells. A cyclic fluctuation in the numbers of T6-positive cells was shown to accompany methotrexate administration on a weekly divided dose schedule.

T cell subsets in human colostrum.

Lymphocytes from 10 paired colostrum and peripheral blood specimens were examined to determine if the colostral T cell population differs from the peripheral blood T cell population in subset distribution. The percentages of lymphocytes staining with OKT3, OKT4, and OKT8 murine monoclonal antibody were determined. Lymphocytes from colostrum were 74.7 +/- 2.5% OKT3+, 50.6 +/- 2.3% OKT4+, 24.0 +/- 1.7% OKT8+, whereas peripheral blood lymphocytes were 78.7 +/- 1.9% OKT3+, 48.4 +/- 1.4% OKT4+, and 29.8 +/- 1.6% OKT8+. The percentage of colostrum lymphocytes positive for OKT3 was significantly although not strikingly lower than the OKT3 percentage for blood lymphocytes (p less than 0.05). This difference was due to the lower percentage of OKT8 positive lymphocytes in colostrum compared with blood (p less than 0.01). Although the T cell subset distribution of colostrum generally appears to be similar to that in the peripheral blood, there were small differences in OKT3 and OKT8 percentages that were statistically significant suggesting the possibility of some selectivity of the colostral T cell population.

Densitometric quantitation of individual phospholipids from natural sources separated by one-dimensional thin-layer chromatography.

A method for the quantitation of small amounts of phospholipids derived from biological sources is described. Total phospholipid is determined by mineralization followed by the estimation of liberated phosphate by means of malachite green. The main phospholipid species are separated by one-dimensional thin-layer chromatography. The individual phospholipids are detected by charring with CuSO4/H3PO4. They may be directly quantitated by scanning the thin-layer chromatography plates with a laser densitometer.

Reduction of the fraction of circulating helper-inducer T cells identified by monoclonal antibodies in psoriatic patients treated with long-term psoralen/ultraviolet-A radiation (PUVA).

Ultraviolet radiation has been found to alter the distribution and function of human lymphocytes. To determine whether photochemotherapy (PUVA) alters circulating levels of T cell subset marker-bearing lymphocytes, cells from 9 patients with psoriasis undergoing PUVA therapy for several years (mean 4.6 +/- 1.4 yr), 17 patients with active untreated psoriasis, and 20 healthy volunteers were reacted with monoclonal antibodies to T cell surface markers, including OKT3 (all peripheral blood T cells), OKT4 (helper/inducer T cells), OKT6 (common thymocytes), and OKT8 (suppressor/cytotoxic T cells), and analyzed by flow cytometry. There were no differences in the distribution of T cell subsets between healthy volunteers and patients with active psoriasis. In contrast, the percentages of lymphocytes reacting with OKT3 and OKT4 were lower (by 16% and 12% percent respectively, p less than 0.0025) in the PUVA-treated patients compared to healthy volunteers or patients with active psoriasis that had not received PUVA therapy. There was no difference in the percentage of OKT8 and OKT6 bearing cells. Squamous cell carcinoma of the skin subsequently developed in 2 of 3 PUVA-treated patients with the lowest percentages of T4-bearing cells. These findings indicate that long-term PUVA therapy is associated with a reduction in circulating helper/inducer T cells. This reduction may have a role in the altered immune function reported in PUVA-treated patients.

Human T-cell function in experimental ascorbic acid deficiency and spontaneous scurvy.

Studies in animal models suggest that ascorbic deficiency impairs T-cell-mediated immunity. We studied five normal volunteers hospitalized on a metabolic unit and consuming a strictly controlled diet deficient in ascorbic acid I) after a 5-wk control period of ascorbic acid supplementation (75 mg/day) and 2) after a 9-wk period of no supplementation. Three of the subjects were restudied after a 5-wk period of ascorbic acid supplementation after the deficient period. At the end of both control periods ascorbic acid levels in plasma ranged from 0.9 to 1.3 mg/dl and in leukocytes from 19 to 30 microgram/10(8) cells. At the end of the deficient period levels of ascorbic acid in plasma ranged from 0.09 to 0.15 mg/dl and in leukocytes from 6.2 to 10 microgram/10(8) cells, levels at or below those frequently found in frank scurvy. None of the T-cell parameters tested including mitogen responsiveness to phytohemagglutinin and percentage of T-cells bearing receptors for IgM (helper cells) and IgG (suppressor cells) was different in the deficient period compared to the control periods. One patient with spontaneous scurvy (plasma ascorbic acid 0.07 mg/dl, leukocytic ascorbic acid 4.9 microgram/10(8) cells) was studied at the time of admission and after vigorous ascorbic acid repletion. All T-cell parameters after repletion were unchanged from admission. We conclude that in man ascorbic acid deficiency, even at the scorbutic level, does not alter T-cell numbers or impair in vitro T-cell function.

[Genetic restrictions of the HGG high-zone tolerance specific suppressive factor: arguments against a direct macrophage involvement (author's transl)]. / Restrictions génétiques du facteur suppressif spécifique dans la tolérance de haute zone à la gammaglobuline humaine et arguments contre un rôle direct des macrophages.

Human gamma-globulin (HGG) high-dose tolerance spleen cell factor is shown to be genetically restricted. Yet, macrophages are not required for its production; and BALB/c mice, whose macrophages are hyperactive, can be tolerized partially by H-2d compatible factor or factor produced by BALB/c mice previously rendered sensitive to tolerance induction by carrageenan pretreatment. Thus, direct, involvement of macrophages in genetic restrictions appears unlikely. Since iron powder treatment unveils an amplifier effect of the crude supernatant from tolerant cells, it is suggested that specific and non-specific amplification coexists with suppression at day 5 of HGG-tolerance induction. Thus, interaction between an IJ+ suppressor T cell and an IJ+ amplifier cell or helper cell (or its precursor) is suggested to account for the observed genetic restrictions.