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PubMed1978

Cellular sensitivity to collagen in rheumatoid arthritis.

We examined patients with rheumatoid arthritis for cellular sansitivity to native human Types I, II and III collagens. Mononuclear cells from 50 patients with rheumatoid arthritis, 21 with other inflammatory arthritides, 20 with osteoarthritis and 20 normal subjects were evaluated for the in vitro production of leukocyte inhibitory factor in response to collagen and a control antigen, streptokinase-streptodornase. By this assay, cells from 37 (74 per cent) and 39 (78 per cent) of the patients with rheumatoid arthritis responded to Types II and III collagens, respectively. In contrast, cells from the 41 patients with other kinds of arthritis and the normal group did not produce this lymphokine to collagens. There was no response to Type I collagen or to denatured alpha chains of these collagens. All four groups responded equivalently to streptokinase-streptodornase. These data demonstrate that most patients with rheumatoid arthritis exhibit cellular sensitivity to Types II and III collagens.

Adult↗

PubMed2005

Alpha-melanocyte-stimulating hormone suppresses antigen-induced lymphocyte proliferation in humans independently of melanocortin 1 receptor gene status.

Studies in mice indicate that alpha-melanocyte-stimulating hormone (alphaMSH) is immunosuppressive, but it is not known whether alphaMSH suppresses human immune responses to exogenous Ags. Human PBMCs, including monocytes, express the melanocortin 1 receptor (MC1R), and it is thought that the ability of alphaMSH to alter monocyte-costimulatory molecule expression and IL-10 release is mediated by this receptor. However, the MC1R gene is polymorphic, and certain MC1R variants compromise receptor signaling via cAMP, resulting in red hair and fair skin. Here, we have investigated whether alphaMSH can suppress Ag-induced lymphocyte proliferation in humans and whether these effects are dependent on MC1R genotype. alphaMSH suppressed streptokinase-streptodornase-induced lymphocyte proliferation, with maximal inhibition at 10(-13)-10(-11) M alphaMSH. Anti-IL-10 Abs failed to prevent suppression by alphaMSH, indicating that it was not due to MC1R-mediated IL-10 release by monocytes. Despite variability in the degree of suppression between subjects, similar degrees of alphaMSH-induced immunosuppression were seen in individuals with wild-type, heterozygous variant, and homozygous/compound heterozygous variant MC1R alleles. RT-PCR of streptokinase-streptodornase-stimulated PBMCs for all five melanocortin receptors demonstrated MC1R expression by monocytes/macrophages, MC1R and MC3R expression by B lymphocytes, but no melanocortin receptor expression by T lymphocytes. In addition, alphaMSH did not significantly inhibit anti-CD3 Ab-induced lymphocyte proliferation, whereas alphaMSH and related analogs (SHU9119 and MTII) inhibited Ag-induced lymphocyte proliferation in monocyte-depleted and B lymphocyte-depleted assays. These findings demonstrate that alphaMSH, acting probably via MC1R on monocytes and B lymphocytes, and possibly also via MC3R on B lymphocytes, has immunosuppressive effects in humans but that suppression of Ag-induced lymphocyte proliferation by alphaMSH is independent of MC1R gene status.

Animals↗

PubMed1978

[Age dependence of immunological methods for detecting an immunodeficiency state (author's transl)].

Cell-mediated and humoral immune responses were studied in 43 healthy volunteers aged between 15--77 years. Besides various skin tests with the antigens candida, trichophyton, mumps, streptokinase-streptodornase, tuberculin, DNCB and KLH also in vitro experiments measuring the immunoglobulin- and complement concentrations, the antibody production to KLH, the lymphocyte transformation rate to PHA, Pokeweed, Con A, PPD were done nearly in all patients. The responsiveness of lymphocytes to PHA and Con A and the sensitization of the skin with DNCB declines in the aged humans, beginning already at the 4th-5th decade. The skin tests with candida, trichophyton were not significantly different in the various age groups. The number of persons with positive skin reactions to the antigens mumps and streptokinase-streptodornase decreased also with advancing age. Lymphocyte transformation and skin test with PPD or tuberkulin were markedly increased beyond the age of 30. Serum levels of immunoglobulins, complement components, the antibody production to KLH, and the lymphocyte transformation rate to Pokeweed were not significantly different in the age groups. Correlation between the tests within each person could not be detected. We made the experience that only a few tests are not enough for the evaluation of an immunodeficient state, but that several tests, a so called TEST BATtery", are necessary.

Adolescent↗

PubMed1976

Delayed hypersensitivity skin testing for assessing anergy in the mid-south.

Although skin testing with ubiquitous antigens is widely employed to assess delayed hypersensitivity, little is known about the effect of geographic location on the frequency of skin test reactions to given antigens. To assess skin test reactivity in the mid-South, 82 hospitalized patients and 68 normal controls had skin tests with six antigens: histoplasmin, mumps, tuberculin purified protein derivative (PPD), Candida, Trichophyton, and streptokinase-streptodornase. Ninety-five percent of normal and 79% of hospitalized subjects without immunologically related disease reacted to at least one of the antigens. A high rate of anergy was found in a clinical setting of debilitation and malnutrition. If subjects in poor condition also were excluded, 93% of hospitalized patients reacted to at least one antigen. Rates of reactivity increased with higher concentrations of antigen. To assess anergy in the mid-South, it is recommended that patients be skin tested initially with histoplasmin, mumps, and PPD antigens. If the patient does not react to any of these, streptokinase-streptodornase and Candida albicans (Dermatophytin "O") should be applied.

Antigens↗

PubMed1976

[Skin tests with phytohaemagglutinin (PHA). Correlation with other parameters of cell-mediated immunity (author's transl)].

100 healthy persons were investigated to find out whether there is a correlation between a lymphocyte stimulation (3H-thymidine incorporation in the lymphocyte transformation test) with phytohaemagglutinin, pokeweed mitogen and concanavalin A and the in vivo reactivity to intracutaneous phytohaemagglutinin application (measured as medium diameter of infiltrates). Further we searched for an influence of positive or negative reactivity to the specific antigens trichophytin, candidin and streptokinase-streptodornase. 1. There is a good qualitative correlation in normal persons between in vitro lymphocyte stimulation by phytohaemagglutinin, pokeweed mitogen and concanavalin A and the medium diameter of infiltrates after intracutaneous application of 2 mug phytohaemagglutinin. Using lower doses of phytohaemagglutinin no such correlation could be found. A quantitative correlation between the medium diameter of infiltrates and lymphocyte transformation by phytohaemagglutinin and pokeweed mitogen cannot be demonstrated. For concanavalin A there is a negative correlation significant at the 99% level. 2. In vivo reactivity to phytohaemagglutinin does not differ in persons with negative and positive reactions to the specific antigens. 3. Lymphocyte stimulation by phytohaemagglutinin, pokeweed mitogen and concanavalin A of persons with positive reactions to trichophytin, candidin and streptokinase-streptodornase is significantly greater than in those with negative reactivity. 4. The results indicate in vivo phytohaemagglutinin testing as a good screening method to judge cell-mediated immunocompetence. The general applicability for differentiation of immunodeficient and immunocompetent patients is to be further investigated.

Adolescent↗

PubMed1975

Delayed cutaneous hypersensitivity and peripheral lymphocyte counts in patients with advanced cancer.

One hundred eighty-three patients with advanced solid neoplasms were tested for their ability to react to four common skin test antigens (tuberculin PPD, streptokinase-streptodornase, mumps, and Monilia) and their ability to develop delayed cutaneous hypersensitivity (DCH) to 2, 4 dinitrochlorobenzene (DNCB). All patients were followed for at least 6 months or until death. Histologic tumor types studied were: melanoma (65), sarcoma (28), squamous cell carcinoma (23), and adenocarcinoma (67). The rate of progression of disease within 6 months of testing was lower in patients who had a positive response to a challenging dose of 50 mug of DNCB. Reactivity to recall antigens had no prognostic value except in patients with adenocarcinomas. Among patients with adenocarcinoma, those who reacted strongly to DNCB and one or more skin test antigens had the best prognosis, while those who were nonreactive to all had the worst prognosis (progression rate: 18% vs. 78%). Peripheral lymphocyte counts were related to the results of DCH to DNCB and skin tests. The preseence or absence of lymphocytopenia (count less than 1000/mm3) had prognostic value in patients who had positive skin test(s). In such patients, the disease progression rate was much higher in patients who were anergic to DNCB and who were lymphocytopenic (90% vs. 40%). These data suggest that DCH to DNCB, recall antigens, and peripheral lymphocyte counts are useful immunologic measurements in patients with advanced cancer. Although the prognostic value of each individual test is relatively limited, the predictive worth can be increased when multiple tests are employed. Pertinent findings reported in the literature are reviewed.

Adenocarcinoma↗

PubMed1985

[Initial clinical results of the prevention of intraoperative adhesions in children].

Postoperatively in 2 to 6% of all cases the result was an intestinal obstruction caused by adhesion. The usual measures were without permanent success. Intraoperatively we applied in 20 children streptokinase-streptodornase in the abdomen. During relaparotomy we saw no adhesions in 40% of these cases, whereas in a control group in all cases adhesions were found.

Abdomen↗

PubMed1975

Abnormalities in cell-mediated immunity in patients with Cryptococcus neoformans infection.

Cryptococcin, streptokinase-streptodornase (SK-SD), mumps, and purified protein derivative (PPD) were used for skin testing and, with whole killed Cryptococcus neoformans, were used in migration inhibition and lymphocyte transformation assays of control subjects and patients with past or present disseminated C. neoformans infection. Cryptococcin was found to differentiate control subjects grouped by known Cryptococcus exposure. Cryptococcin and C. neoformans were effective in stimulating leukocyte migration inhibition and lymphocyte transformation in the cryptococcin skin test-positive control subjects. Fifteen apparently normal patients who had been cured of cryptococcosis were found, as a group, to have impaired responsiveness to skin testing with cryptococcin and mumps, minimal leukocyte migration inhibition when stimulated with cryptococcin or C. neoformans, but normal group responses to cryptococcin in Cryptococcus-induced lymphocyte transformation. Six patients with known predisposing conditions to disseminated infection (sarcoid, lymphoma, leukemia, steroid therapy) had markedly diminished responses to most skin tests and in vitro assays. It is suggested that the apparently normal individual who develops disseminated cryptococcal infection has subtle defects in cellular immunity that may have antedated and predisposed to infection.

Antigens, Fungal↗

PubMed1975

Depression of cell-mediated immunity in atopic eczema.

Prompted by recent observations that the thymus exerts an important regulatory influence over IgE antibody production in lower species, we conducted studies of immune function in 21 patients with atopic eczema to seek evidence for a similar relation in man. Skin tests for delayed hypersensitivity to Candida albicans and streptokinase-streptodornase (SK-SD) revealed a striking degree of anergy that correlated with the severity of the eczema. A correlation was also noted between the extent of the dermatitis and the magnitude of the serum IgE concentration. Other immunologic abnormalities did not appear related to the severity of eczema put pertained to the group as a whole. These included significantly (p = less than 0.0001) lower mean percentages of spontaneous sheep erythrocyte (E) or T cell rosettes and of rosettes with neuraminidase-treated sheep erythrocyte (En) rosettes, and significantly lower in vitro lymphocyte responsiveness of the mitogens concanavalin A (p = 0.0013) and poleweek mitogen (p = 0.0002) and to Candida antigen (p = 0.0017) than in normal subjects. Responses to phytohemagglutinin and tetanus toxoid were also depressed but differences were not statistically significant. An increased percentage (p = 0.0324) of peripheral blood B lymphocytes bearing the complement receptor was noted, but, except for a slight increase in lymphocytes bearing IgD, percentages of lymphocytes bearing other immunoglobulins (including IgE) were not elevated.

Adolescent↗

PubMed1975

The effect of aging and acute illness on delayed hypersensitivity.

A group of standard antigens (monilia, mosquito, mumps, purified protein derivative [PPD], staphylococcus toxoid, streptokinase-streptodornase [sk-sd] and trichophyton) were applied to 321 normal volunteers, 60 patients admitted to a medical ward, and 41 patients in an intensive care unit (ICU) to evaluate their delayed hypersensitivity skin test response. Eighty-eight per cent of the normal subjects reacted with at least 5 mm. induration to one or more skin tests without any decrease in reactivity occurring with increasing age. In the hospitalized group, only 62 per cent of the ward and 63 per cent of the ICU patients reacted to the same skin tests. All (8/8) anergic ICU patients tested after discharge regained normal reactivity. Acute illness but not increasing age will impair the delayed hypersensitivity skin test response.

Acute Disease↗

PubMed1980

In vivo and in vitro cell-mediated immunity to tetanus toxoid in adults.

The purpose of this study was to evaluate tetanus toxoid (TT) as an indicator of cutaneous delayed hypersensitivity (CDH) in adults. Fifty-two normal subjects, aged 25 to 64 yr, were skin tested with TT and streptokinase-streptodornase (SK/SD). Lymphocyte transformation was studied in seven normal TT reactors, four normal TT nonreactors, and seven hospitalized anergic patients. CDH was common with both TT and SK/SD; 90% of the adults, aged 25 to 39 yr, had CDH reactions to TT and 79% had CDH reactions to SK/SD. In adults aged 40 to 64 yr, 75% had DCH reactions to TT and 59% had CDH reactions to SK/SD. Lymphocyte transformation to TT correlated well with TT skin-test results. Punch biopsy specimens of TT reactions 48 hr after skin testing demonstrated DCH. We conclude that TT is an excellent antigen for assessing the presence or absence of CDH in adults aged 25 to 64 yr.

Adult↗

PubMed1981

Role of cell-mediated immunity in Hymenoptera allergy.

Currently there is little information regarding the immunologic mechanisms responsible for large local reaction (LLR) after Hymenoptera stings. To investigate this question, we measured in vitro lymphocyte proliferation and delayed skin reactivity to venom antigens in 10 subjects with LLR (six with LLR only and four with LLR and systemic reactions), seven subjects with systemic reactions, and eight nonallergic controls. The lymphocyte response to venoms in the LLR group was greater than that in either the systemic reactor group (p less than 0.05) or the control group (p less than 0.001). In contrast, lymphoproliferative responses to Candida albicans, streptokinase-streptodornase, and phytohemagglutinin were comparable in the three groups. Forty percent of the LLR group had positive delayed skin tests to venom antigens, and none of the patients in the systemic reactor group had such responses. These findings suggest that cellular immune mechanisms play a role in the pathogenesis of LLR after Hymenoptera stings.

Candida albicans↗

PubMed1982

Collagens act as ligands to stimulate human monocytes to produce mononuclear cell factor (MCF) and prostaglandins (PGE2).

Blood mononuclear cells from patients with rheumatoid arthritis produce the lymphokine, leukocyte inhibitory factor (LIF) in response to collagens in vitro, and blood monocytes release prostaglandins (PGE2) and a factor, mononuclear cell factor (MCF) which stimulates collagenase and PGE2 production by cultured synovial cells. We therefore examined the effect of collagens on the production of PGE2 and MCF. Blood mononuclear cells from 6 patients with rheumatoid arthritis and 6 normal subjects were cultured in native human types I, II, or III collagen-coated tubes, or with streptokinase-streptodornase (SK-SD), and the supernatant media derived from these cultures analyzed for the presence of MCF, PGE2, and LIF. Types II and III collagens, as well as SK-SD, markedly stimulated MCF production by the cells from all 12 subjects (MCF activity, expressed as a mean stimulation index (SI) +/- SEM, was 43 +/- 12 for type II, 33 +/- 7 for type III, and 37 +/- 23 for SK-SD). Type I collagen was less stimulatory (mean SI 10 +/- 7). Cells from the patients with rheumatoid arthritis, but not the normal subjects, produced LIF in response to types II or III collagens but not to type I collagen. PGE2 production by blood mononuclear cells paralleled that of MCF, although abrogation of PGE2 release with indomethacin did not reduce MCF production. alpha chains purified from denatured collagens also stimulated MCF production. Using cells from patients with rheumatoid arthritis, type II collagen stimulated production of all three factors in the presence of polymyxin B or fibronectin-depleted serum, suggesting, respectively, that neither endotoxin nor fibronectin were responsible for their generation. Monocytes, purified from normal blood by an adherence technique, but not lymphocytes depleted of monocytes, released MCF and PGE2 when cultured with type II collagen. These results demonstrate that collagens can act as ligands to stimulate monocytes, as well as antigens to stimulate sensitized lymphocytes, to produce soluble factors that may contribute to the destruction of connective tissue.

Arthritis, Rheumatoid↗

PubMed1974

Effect of normal and activated human macrophages on Toxoplasma gondii.

Human macrophages derived from in vitro culture of peripheral blood monocytes were studied under a variety of conditions to determine their microbicidal capacity for the obligate intracellular protozoan, Toxoplasma gondii. The effect of macrophages on intracellular Toxoplasma was evaluated morphologically by light and phase microscopy and by autoradiography. When macrophages from dye test (DT)-negative or DT-positive individuals were infected with Toxoplasma in the presence of normal human serum, the organisms were able to multiply intracellularly with resultant destruction of the monolayer. Once organisms were intracellular, the presence of antibody-containing serum in the medium did not alter this inability of the macrophages to kill Toxoplasma. However, when Toxoplasma were incubated in the presence of heat-inactivated DT-positive serum just before infection of the monolayers, the intracellular organisms were inhibited or killed by normal macrophages. Attempts were made to activate macrophages in vitro to kill Toxoplasma. Macrophages incubated in the presence of sensitized lymphocytes and Streptokinase-Streptodornase (SK-SD) or Toxoplasma lysate antigen (TLA) were found to kill Toxoplasma when compared to macrophages incubated in the presence of lymphocytes from DT-negative individuals and TLA or lymphocytes alone. Thus, in vitro induction of resistance (both specifically and nonspecifically) in human macrophages was accomplished by culturing these cells in the presence of specifically sensitized lymphocytes and antigen. These results suggest that, as in the mouse model, activated human macrophages have the ability to inhibit or kill intracellular Toxoplasma and that these cells may be important as effector cells in cell-mediated immunity (CMI) to toxoplasmosis in man.

Adolescent↗

PubMed1974

Studies on mediator production by highly purified human T and B lymphocytes.

Highly purified populations of T and B lymphocytes obtained by affinity column separation were stimulated by antigen and their ability to produce two mediators, migration inhibitory factor (MIF) and lymphocyte mitogenic factor (LMF) was assessed. Both T- and B-cell populations made MIF; the production of MIF was antigen-specific using purified protein derivative of tuberculin, streptokinase-streptodornase, and Candida antigens. The MIF activity from both populations could not be attributed to antigen-antibody complexes as the inhibitory activity eluted from Sephadex G-100 columns in the same region corresponding to mol wt 23,000 daltons. Further studies indicate that the T cells producing MIF are proliferating cells whereas the B cells producing this mediator are not. In contrast, LMF was made only by T cells and not B cells when these populations were stimulated by antigen. The LMF induced the [(3)H]thymidine incorporation into both T and B cells obtained from donors lacking sensitivity to the antigens used to elicit the factor. Chromatographic studies indicate that LMF eluted from Sephadex G-100 in a fraction of mol wt 23,000 daltons where MIF is also found; however, since B cells produce MIF but not LMF, these two factors appear to be distinct from one another. Some of the implications of these findings are discussed. The explanation for the production or lack of production of MIF by lymphocytes obtained from patients with immunodeficiency disorders requires reinterpretation.

Antigen-Antibody Reactions↗

PubMed1976

Requirement of precommitted cells as targets for the augmentation of lymphocyte proliferation by leukocyte dialysates.

After our initial report tha leukocyte dialysates containing transfer factor augment the thymidine incorporation of antigen-stimulated lymphocytes, we have adapted the system to microleukocyte cultures. This modification permits both (a) the simultaneous assay of a single dialysate on the cells of multiple individuals, and (b) the assay of multiple dialysates on the cells of a single individual. The data thus secured, demonstrate that dialysates from both skin-test-positive and -negative donors produced similar degrees of augmentation whether the data are expressed as an arithmetic difference or as a ratio. When expressed as an arithmetic difference, the amount of augmentation is increased in proportion to the level of thymidine incorporation of the assay cells when they were stimulated by antigen alone. When expressed as a ratio, however, the degree of augmentation is independent of the response of the assay cells. An analysis of the ability of dialysates to engage previously uncommitted lymphocytes and thus to augment thymidine incorporation, revealed that precommitted cells were required. In these experiments, antigen-reactive cells were deleted from populations of peripheral blood lymphocytes by incubation with purified protein derivative of tuberculin, diphtheria toxoid, or streptokinase-streptodornase in the presence of [3H]thymidine of high specific activity. This deletion depressed or abolished the effect of dialysate on the residual population when it was recultured with the same antigen, but the effect on the response of the remaining lymphocytes to other antigens was unaltered. In this study, leukocyte dialysate appeared to augment nonspecifically the thymidine incorporation of an antigen-specific precommitted clone of lymphocytes. The relationship of these adjuvant effects on peripheral blood lymphocytes in vitro to the specific and nonspecific activities of transfer factor in vivo remains to be elucidated.

Adjuvants, Immunologic↗

PubMed1982

Modulation of human lymphocyte function by C3a and C3a(70-77).

Human C3a and the synthetic octapeptide C3a (70-77), which retains the activities of an anaphylatoxin, inhibit in a concentration-dependent manner the generation of leukocyte inhibitory factor (LIF) activity by human mononuclear leukocytes and T lymphocytes cultured with the mitogens phytohemagglutinin (PHA) or concanavalin A (Con A) or the antigen streptokinase-streptodornase (SK-SD). The generation of LIF activity was inhibited by 50% by 10(-8) M C3a or C3a(70-77) with PHA or Con A as the stimulus, whereas a more than 10-fold higher concentration of C3a(70-77) than C3a was required to achieve the same level of suppression with SK-SD as the stimulus. Similar concentrations of C3a(70-77) inhibited to the same extent the migration of T lymphocytes stimulated by alpha-thioglycerol of Con A. Neither C3a nor C3a(70-77) altered significantly the uptake of [3H]thymidine by human mononuclear cells exposed to PHA, Con A, or SK-SD. The capacity of C3a(70-77)-Sepharose,m but not Sepharose alone, to adsorb or inactivate mononuclear leukocytes required for the generation of LIF activity established a direct interaction. Analysis of the lymphocytes in the effluent from C3a(70-77)-Sepharose columns, using monoclonal antibodies to surface antigens, showed a selective depletion of the helper/inducer population of lymphocytes. C3a might represent an important mediator of the functionally selective regulation of human T lymphocyte activities by the complement system.

Cell Division↗

PubMed1977

Cell-mediated immune responses in humans after induced infection with influenza A virus.

Cell-mediated immune responses were examined in 19 normal volunteers after intranasal administration of three strains of influenza A virus. Eight volunteers manifested respiratory tract illness along with fourfold rises of serum antibody and/or virus shedding. Samples of peripheral venous blood were obtained before and two days, five days, and four weeks after challenge. During acute illness, infected volunteers showed lymphopenia, which persisted for up to four weeks after challenge. The lymphopenia involved thymus-derived, bone marrow-derived, and null cells. Blastogenic responses of lymphocytes to stimulation with phytohemagglutinin, concanavalin A, and streptokinase-streptodornase were depressed during acute illness, and responses to phytohemagglutinin and concanavalin A remained depressed at four weeks after infection. Thus, influenza infection in humans can result in prolonged depression of numbers and functions of circulating lymphocytes.

Adolescent↗