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Results for “Hypersensitivity, Delayed”

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At least 145 records · Page 8Linked to original sources
PubMed1983

Delayed hypersensitivity response and vitamin D deficiency.

The relationship between delayed hypersensitivity and serum levels of 25-hydroxyvitamin D were examined in sixty-three elderly people. After intracutaneous injection of five recall antigens (Candida, mumps, PPD, tricophyton and varidase) nineteen subjects showed no response (anergy), seven showed only a weak reaction (relative anergy), and thirty-seven a normal reaction. In the anergic group mean serum level of 25-hydroxyvitamin D was significantly lower than in the group with normal immunoreactivity. Five subjects with anergy and serum 25-hydroxyvitamin D below 20 nmol/l were treated with oral vitamin D or UV irradiation for two to three months, after which both the serum 25-hydroxyvitamin D levels and the delayed hypersensitivity were normalized. In a non-treated group anergy persisted in seven out of nine patients in a second skin test. We conclude that anergy in the delayed hypersensitivity skin test in humans may in some cases be due to vitamin D deficiency.

25-Hydroxyvitamin D 2↗
PubMed1984

Unequivocal delayed hypersensitivity in mast cell-deficient and beige mice.

It has been suggested that reserpine blocks expression of delayed hypersensitivity in mice because it depletes stores of the vasoactive amine serotonin in mast cells. To determine whether mast cell serotonin or other mast cell-derived mediators are essential for delayed hypersensitivity, responses to contact sensitizers in mast cell-deficient W/Wv or Sl/Sld mice were studied. Because blood platelets represent another potential source of serotonin in delayed hypersensitivity responses, beige mice, whose platelets contain less than 1 percent of the normal levels of serotonin, were also examined. By the criteria of tissue swelling, infiltration of iodinated leukocytes, or histology, mast cell-deficient or beige mice expressed delayed hypersensitivity reactions whose intensity generally equaled or exceeded that of reactions in littermate controls. In addition, reserpine blocked delayed hypersensitivity in W/Wv and beige mice, suggesting that effects on mast cell or platelet serotonin cannot explain this drug's action in delayed hypersensitivity.

Animals↗
PubMed1966

Selective suppression of delayed hypersensitivity by the induction of immunologic tolerance.

Administration of DNP-BGG to newborn guinea pigs resulted, in more than half of the animals, in the specific suppression of delayed hypersensitivity to DNP-BGG and BGG, as shown after immunization with DNP-BGG in complete Freund's adjuvant. In contrast, all animals formed antibodies to DNP-BGG, whether or not delayed hypersensitivity to this antigen was present. No difference in antibody titers was found between pretreated and control animals. All animals had antibodies reacting specifically to the hapten DNP, and most of them to the carrier protein BGG, whether or not delayed hypersensitivity to the carrier protein was present. Furthermore, some animals with and without positive 24 hr skin test to DNP-BGG had antibodies with a combined hapten-carrier protein specificity to this antigen, i.e., a specificity which is similar to that of delayed hypersensitivity. Thus, delayed hypersensitivity and antibody formation to similar antigenic determinant were differently affected by injection of antigen in the neonatal period. The finding that delayed hypersensitivity and antibody formation could be dissociated by the induction of immunologic tolerance supports the assumption that delayed hypersensitivity and antibody formation are different immune processes which are not necessarily linked together.

Anaphylaxis↗
PubMed1975

Delayed hypersensitivity to influenza virus in man.

Delayed hypersensitivity to influenza antigen has been demonstrated in man by means of skin tests and 'in vitro' lymphocyte transformation. Adjuvanted influenza vaccine enhances this response, in contrast to non-adjuvanted vaccine in commercial use.

Antibodies, Viral↗
PubMed1975

Delayed hypersensitivity in patients with bronchial carcinoma.

Delayed hypersensitivity skin test reactions have been carried out in patients with bronchial carcinoma. Dinitrochlorobenzene, used as a parameter of newly induced cell-mediated immunity, was clearly suppressed, and this suppression was associated with a poor prognosis. Tuberculin reactivity, used as a parameter of the memory function of the cell-mediated immune system, was not altered, and bears no relation to prognosis.

Adenocarcinoma↗
PubMed1980

Release of an endogenous pyrogen from guinea pig leukocytes: the role of T lymphocytes and correlation with suppression (desensitization) of delayed hypersensitivity.

The pathogenesis of fever in delayed hypersensitivity (DH) was studied in guinea pigs immunized with either ovalbumin or bovine gamma-globulin in complete Freund's adjuvant. In vitro incubation of sensitized lymphocytes with the specific antigen used for immunization resulted in the elaboration of a lymphokine-like factor that activated either monocytes or neutrophils to release endogenous pyrogen (EP), the protein that causes fever. Specifically sensitized T cells appeared to be responsible for release of this EP-inducing factor. Desensitization of the dermal DH response to antigen was produced by several large injections of antigen and was associated with a reduced capacity of lymphocytes from such animals to activate phagocytic cells to release EP. This may explain the reduced fever (pyrogenic tolerance) that occurs when repeated injections of antigen are given to sensitized animals. Fever and the dermal response to DH seem to be closely linked reactions that have evolved to defend the host against invading pathogens. In both reactions, phagocytic cells appear to be activated by lymphokines derived from T lymphocytes specifically responding to microbial antigens.

Animals↗
PubMed1977

The delayed hypersensitivity response: application in clinical surgery.

Delayed hypersensitivity skin testing was performed on 520 surgical patients. Significantly higher incidences of sepsis and mortality (p less than 0.001) were found in the abnormal patients as compared to normal responders in the preoperative (322 patients), postoperative and post-trauma (115 patients), and nonoperative (83 patients) groups. Sequential testing in individual patients was of even greater prognostic value. Of the 177 patients who either remained normal or whose responses became normal, the sepsis rate was 10.1%, and the mortality rate was 8.4%. However, a sepsis rate of 57.6% and a 78% mortality rate were found in those patients who developed abnormal responses or whose responses did not improve. Cancer and increased age (older than 80 years) did not account for the incidence of anergy and relative anergy. The mortality rate was higher in the cancer group. Anergy and relative anergy were found to be associated with malnutrition, sepsis, shock, and trauma. In the clinical setting, effective treatment of these associated conditions, especially the maintenance of body cell mass by the use of total parenteral nutrition, was associated with reversal of the anergic state and an improved prognosis.

Adolescent↗
PubMed1969

Study of delayed hypersensitivity to myxoviruses induced by vaccines.

The delayed hypersensitivity response of guinea pigs to Bacillus Calmette-Gúerin (BCG) and myxovirus vaccines was investigated by use of the techniques of skin testing and inhibition of macrophage migration. A serum antibody response to the injected vaccines was readily demonstrable. Parainfluenza type 2 virus consistently failed to induce a delayed hypersensitivity state in 15 animals, even with the use of a virus adjuvant emulsion. Respiratory syncytial virus occupied an intermediate position in that positive delayed type skin tests of an erythematous nature were elicited following inoculation, but only two of seven guinea pigs yielded a positive migration inhibition test. In mumps-inoculated animals, skin testing gave rise to erythematous delayed skin reactions which varied from 0 to 20 mm in size. Migration inhibition could be demonstrated in 7 of 21 animals. In almost all guinea pigs inoculated with BCG, large, indurated, erythematous skin reactions were elicited, and inhibition of macrophage migration was readily demonstrated. The degree of skin reactivity was positively correlated with inhibition of macrophage migration. If the skin reaction to a specific antigen exceeded 9 mm of erythema, that antigen also inhibited macrophage migration. Skin testing proved to be the most sensitive indicator of viral hypersensitivity. Migration inhibition was demonstrated only when a greater than 8-mm skin reaction was evoked. This cellular hypersensitivity appeared to be a qualitative phenomenon, the expression of which could be heightened by the use of adjuvant. The applicability and sensitivity of the migration inhibition technique is considered relative to its use for in vitro monitoring of effects of viral vaccine inoculations.

Adjuvants, Immunologic↗
PubMed1975

Rosette-forming ability of thymus-derived lymphocytes in cell-mediated immunity. I. Delayed hypersensitivity and in vitro cytotoxicity.

Effector cells in delayed hypersensitivity and in vitro cytotoxicity were studied in lymph node cells from animals immunized with sheep erythrocytes (SRBC) in complete Freund's adjuvant. Delayed hypersensitivity response (DHR) was assayed by the increase in foot pad swelling after the intrafoot pad injection of immune cells plus antigen. Cell-mediated cytotoxicity against SRBC was assayed by a microcytotoxicity test with sheep fibroblasts as target cells. Effector cells were antigen specific, sensitive to anti-theta serum plus complement (C), and insensitive to anti-Ig serum plus C. A nonrosette-forming (non-RFC) small lymphocyte effector T cell and a rosette-forming medium lymphocyte effector T cell were isolated by velocity sedimentation. The small lymphocyte non-RFC required a longer time than the medium lymphocyte RFC effector cell to produce maximum activity. Buoyant density failed to distinguish medium lymphocyte effector cells in DHR and in vitro cytotoxicity.

Animals↗
PubMed1987

Cellular kinetics of delayed hypersensitivity test reactions to topical glucocorticosteroids.

The phenotypes of the infiltrating cells in 13 patients with delayed hypersensitivity to topical glucocorticosteroids (GCS) were studied from sequential biopsies of positive epicutaneous test reactions by using the avidin-biotin-complex (ABC) technique. Monoclonal antibodies were used to identify the cells with the following phenotypes: T3, T4/T4a, T6, T8, T9, T11, M1, Ia1 (HLA-DR), interleukin-2 receptor/T26a, and dendritic reticular cell. The cellular kinetics of GCS hypersensitivity reactions were compared with delayed hypersensitivity reactions caused by allergens not related to GCS. In both GCS and non-GCS reactions the epidermal dendritic T6+ cells were more numerous than dendritic Ia1+ cells. There was a decrease in the number of both cell types during these reactions; in GCS reactions the decrease in the number of T6+ cells was seen later than in non-GCS reactions. Ia1+ keratinocytes were seen at sites near dermal infiltrates. Compared with the non-GCS delayed hypersensitivity reaction, there were fewer pan T (T11+/T3+) in the GCS reaction. The relative numbers of M1+ monocytes and the T4/T8 ratio were substantially lower in the latter; these findings can be explained as a GCS effect which modulates the delayed type hypersensitivity reaction.

Administration, Cutaneous↗