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At least 199 records · Page 11Linked to original sources
PubMed1985

Effects of antiarthritic compounds on sheep erythrocyte-induced delayed-type hypersensitivity.

Delayed hypersensitivity (DTH) to sheep erythrocytes (SRBC) in mice is a simple model of cellular immunity mediated primarily by Ly 1+ T-cells. Because little is known about the pharmacology of this model, the therapeutic effects of a variety of antiarthritic agents were tested. Swelling was determined using mercury plethysmography and used to determine drug activity. Two immunosuppressive agents (cyclophosphamide and azathioprine) and two steroids (dexamethasone and hydrocortisone) significantly reduced swelling. Only one of six nonsteroidal antiinflammatory drugs (NSAIDs), aspirin, reduced swelling. Indomethacin, phenylbutazone, and benoxaprofen augmented swelling and ibuprofen and isoxicam were inactive. Four disease-modifying antirheumatic drugs (DMARDs), D-penicillamine, levamisole, chloroquine, and aurothioglucose, were tested and none inhibited swelling. Aurothioglucose significantly augmented swelling. In conclusion, only steroids and immunosuppressive agents had consistent effects on DTH to SRBC. In general, NSAIDs and DMARDs were either inactive or augmented swelling. These results suggest that this model may be of use as a routine screen for immunomodulatory agents.

Animals↗
PubMed1992

[Postoperative complications and mortality; results of skin tests in delayed hypersensitivity].

In 221 patients the test of cutaneous delayed hypersensitivity was done before the operation and 4 days after it, using 3 antigens: tuberculin, distreptase and phytohaemagglutinin. The patients were divided into three groups: I control (109) subjected to minor and moderately serious operations, and study group (II) with peritonitis (IIa 40 cases), digestive tract cancer (IIb 65 cases) and digestive tract diseases (IIc 7 cases). The study showed that in cases with preoperative anergy to antigens the operations were followed significantly more frequently by serious septic complications and mortality from these complications was much higher. No patients with preoperatively normal responses to the antigens died after the operations. The test makes possible preoperative detection of high surgical risk connected with infection, and early treatment reducing postoperative mortality.

Adolescent↗
PubMed1977

Specific restoration of delayed hypersensitivity by lymphoid tissue extracts.

Mice lose demonstrable delayed hypersensitivity (DH) to DNFB, picryl chloride, or sheep red blood cells. Reconstitution of immune responsiveness can be accomplished by administration of cell-free lysates of spleens from mice with active DH to structurally related, but not to unrelated antigens. Peritoneal exudate cell lysates from mice with active DNFB-DH also restore DH to this antigen. Sera from sensitized mice, and sera and lymphoid tissue extracts from unsensitized mice are without activity. The restorative property of splenic lysates from DNFB-sensitized mice is unstable at 56 degrees C, not sedimented at 90,000 X G and inactivated by trypsin or magnesium ions. The presence of unexpressed, restorable DH may provide a biologic basis for the so called "transfer factor" phenomenon.

Animals↗
PubMed1976

Local adoptive transfer to mice of human delayed hypersensitivity: reactions by the radioisotopic footpad assay.

Human delayed hypersensitivity to living BCG organisms and/or Varidase was adoptively transferred to mice and assayed in mice by a radioisotope footpad assay (FPA). A mixture of the antigen and peripheral blood lymphocytes from patients (positive skin reactions to PPD and/or Varidase) or healthy volunteers was inoculated into the footpads of lethally X-irradiated mice. A positive footpad reaction was accompanied by an increased leakage of the radiolabelled serum protein from the blood stream into the intercellular space at the site of inoculation, and was measured by the 'foot-count ratio', or radioactivity in the test foot divided by radioactivity in the contralateral foot. The intensity of the footpad reaction correlated directly with the skin test response of the human lymphocyte donors.

Adolescent↗
PubMed1984

A high-molecular-weight trypsinlike protease in the skin sites of delayed hypersensitivity in guinea pigs.

A trypsinlike protease was extracted from the delayed hypersensitivity skin sites in guinea pigs. Extractable amounts of the enzyme were chronologically paralleled with the gross appearance of the inflammation, and the maximum activity from the inflamed sites at 24-36 hours was about 20 times stronger than that from normal skin, suggesting a potential role in the pathogenesis of the delayed hypersensitivity reaction. The enzyme, which suitably hydrolyzed t-butyloxycarbonyl-phenylalanyl-seryl-arginine 4-methylcoumaryl-7-amide, was partially purified by isoelectric focusing or by gel filtration. The enzyme demonstrated a single peak of activity on the former column with an apparent isoelectric point of 4.2, and in the latter it showed an apparent molecular weight of 600,000 (600K-protease). When incubated with 3H-diisopropylfluorophosphate, the enzyme lost all amidolytic activity and yielded a single band of radioactivity in polyacrylamide disk gel electrophoresis in the presence of sodium dodecyl sulfate, and a single peak of radioactivity in gel filtration, both having an apparent molecular weight of 31,000-33,000 (31K-protease). That the 600K-protease might be a complex with alpha 2-macroglobulin was ruled out. The 31K-protease was separated from the 600K-protease by gel filtration in the presence of 6 M guanidine hydrochloride, and was renatured to an active form. An apparent isoelectric point of the 31K-protease observed was 9.4, suggesting that the 600K-protease may be a complex of 31K-protease with an acidic carrier molecule(s). Both proteases, 31K- and 600K-protease, had identical substrate specificity, a pH profile of amidolytic activity, and susceptibility to exogenous protease inhibitors. However, when sensitivities to intrinsic protease inhibitors in guinea pig plasma, two kinds of trypsin inhibitor, and alpha 2-macroglobulin were compared, the 600K-protease was at least 100 times more resistant than the 31K-protease. It was supposed that one of the pathophysiologically significant functions of the complex formation might be to maintain the enzyme activity longer in vivo.

Amidohydrolases↗
PubMed1980

Assessment of immediate and delayed hypersensitivity skin tests with Schistosoma mansoni adult worm antigen in a rural Egyptian population.

Immediate and delayed hypersensitivity responses to schistosome adult worm skin test antigen were assessed in 418 farmers in Dakahlia Governorate, Egypt. All were from a population frame being epidemiologically evaluated for bilharzial urinary bladder cancer and thus were all 20 years old or older. A control, group of 108 adult urban dwellers without antecedent or current history of schistosomiasis were also tested. Ninety eight percent (411/418) of farmers and 35% (38/108) of controls showed reaginic hypersensitivity to 20 micrograms protein antigen. While 43% (180/418) of farmers and 4.6% (5/108) of controls showed positive delayed responses. Schistosoma haematobium eggs were found in 6% on urine cytology smears (Papanicolaou) and in 5% by Nuclepore filtration. A subsample of 97 individuals showed 21% to have S. haematobium eggs in urine by a traditional sedimentation technique. Immediate skin tests were equally positive in egg positive or egg negative farmers but delayed responses were 55% positive in the former and 26% in the latter. It is suggested that the delayed hypersensitivity skin test may be more specific and useful in epidemiologic surveys. The changing prevalence of S. haematobium infections in the Nile Delta is briefly discussed.

Adult↗
PubMed1985

A new method of eliciting delayed hypersensitivity in the mouse abdominal cavity.

A new method of determining delayed hypersensitivity quantitatively was investigated in mice. Mice were sensitized with 150 micrograms of ferritin and, 3 weeks later, antigen challenge was performed by implanting a sponge containing antigen in the abdominal cavity. Cells accumulated in the sponge markedly increased in number for 24-72 h after the challenge; mononuclear cells predominated by 48 h. When sensitized lymphocytes were transferred passively to a normal recipient, marked cell accumulation in the sponge was found 48 h after the challenge. Immunological specificity was confirmed in animals sensitized to antigen and receiving passive transfer of sensitized cells. Strain differences in this reaction were observed. Cortisone (20 mg/kg for 6 days before challenge) significantly decreased cell accumulation. Delayed hypersensitivity was also elicited in the ear of sensitized animals. Extracts of sponges removed from antigen-challenged mice had macrophage chemotactic activity.

Animals↗
PubMed1982

Transfer of Salmonella resistance and delayed hypersensitivity with murine-derived transfer factor.

Protective host immunity and delayed hypersensitivity were transferred to nonimmune ICR and C3H/HeJ mice with transfer factor prepared from the splenic lymphocytes of ICR Swiss mice immune to Salmonella typhimurium. Only mice injected with the "immune" dialysate exhibited significant footpad swelling (P less than 0.01) to a spent medium antigen of S. typhimurium, but not Listeria monocytogenes. Host survival to a lethal Salmonella challenge infection was seen only in transfer factor-injected mice. Also, these challenged animals had fewer numbers of bacteria present in their spleens (P less than 0.01) than did challenged mice previously injected with either control dialysates or commercial endotoxin. Neither the Salmonella antigens nor endotoxin present in the sterile transfer factor preparation was responsible for the transfer of host protection and delayed hypersensitivity, since none of the control dialysates resulted in any positive responses when injected into either the ICR Swiss or endotoxin-resistant C3H/HeJ mice.

Animals↗
PubMed1982

[Parallel formation of delayed-hypersensitivity effectors and T-suppressors in the intraperitoneal administration of a massive dose of ram erythrocytes].

Injection of 6 X 10(9) sheep red blood cells (SRBC) to mice led to parallel formation, on days 4-5, of delayed hypersensitivity effector cells (the activity was tested in local transfer experiments) and delayed hypersensitivity T-suppressors preventing sensitization of syngeneic recipients. After massive injection of SRBC the activity of spleen suppressors gave 2 peaks: on days 5 and 14. Five days after massive antigen injection only T-cells capable of sorbing on a specific antigen manifested suppressor activity. On day 14 T-cells capable of sorbing on specific antibodies showed a specific activity, whereas T-cells capable of sorbing on a specific antigen retained only part of their activity. The mechanism of delayed hypersensitivity inhibition following massive antigen injection by suppressors obtained by day 5 is reviewed in terms of Germain and Benacerraf's theory postulating that delayed hypersensitivity is regulated by Ly 2+, I-J+ antiidiotypic suppressors capable of sorbing on specific antibodies and formed upon injection of Ly 1+, I-J+, Id+ inductor cells capable of sorbing on a specific antigen.

Animals↗
PubMed1995

A monoclonal antibody to cis-urocanic acid prevents the ultraviolet-induced changes in Langerhans cells and delayed hypersensitivity responses in mice, although not preventing dendritic cell accumulation in lymph nodes draining the site of irradiation and contact hypersensitivity responses.

Ultraviolet B (UVB) irradiation of C3H mice causes suppression of delayed hypersensitivity and contact hypersensitivity (CH) to antigens encountered following exposure, and is accompanied by a reduction in Langerhans cell (LC) numbers in the epidermis, loss of epidermal antigen-presenting cell function, and accumulation of dendritic cells in lymph nodes draining the site of irradiation. Various photoreceptors and mediators of these changes have been proposed, one of which is cis-urocanic acid (cis-UCA) formed from the naturally occurring trans-UCA in the epidermis on UV irradiation. A monoclonal antibody that reacts with cis-UCA has become available recently and has been used in this study to clarify the role of UCA. Pretreatment of C3H mice with the monoclonal antibody abrogated the UVB-induced and cis-UCA-induced reduction in epidermal LC numbers. It also prevented the UV-induced suppression of epidermal antigen-presenting cell ability as measured by the mixed skin lymphocyte response. However, it had no effect on the accumulation of dendritic cells in lymph nodes draining the site of UV exposure. With regard to hypersensitivity responses, it did not prevent UV-induced suppression of CH to oxazolone at a range of concentrations but it restored to normal the UV-suppressed delayed hypersensitivity to herpes simplex virus, if administered before exposure. Thus cis-UCA is involved in some UV-induced changes in murine skin but not in others, where alternative mediators, such as tumor necrosis factor-alpha, may be more important.

Animals↗
PubMed1979

Development of delayed hypersensitivity responses in Mycobacterium lepraemurium infections in resistant and susceptible strains of mice.

C57Bl mice are relatively resistant to a moderate subcutaneous infection with Mycobacterium lepraemurium while BALB/c mice are much more susceptible. Cutaneous delayed hypersensitivity reactions which develop in the first 3 weeks of infection were compared in these two strains of mice. Both strains gave a peak of delayed hypersensitivity between 6 and 10 days after infection which was followed by a period of low reactivity before the development, in the third week, of a stable persistent delayed hypersensitivity reaction. There was no difference between the strains in the size at 24 h of the delayed hypersensitivity reaction but the reactions differed in their kinetics. The low resistance strain, BALB/c, gave a Jones-Mote-type of response while the high resistance strain gave a response which could be described as a tuberculin-type reaction.

Animals↗
PubMed1983

Membrane phenotype of murine effector and suppressor T cells involved in delayed hypersensitivity and protective immunity to herpes simplex virus.

The membrane phenotype of T cells involved in delayed hypersensitivity (DH), protective immunity, and suppression of delayed hypersensitivity to herpes simplex virus (HSV) has been determined. T cells from immune lymph nodes transferring DH and antiviral immunity to normal recipients were characterized as Lyt 1+2-. There appeared to be no detectable antiviral role for Lyt 1-2+ cells in the transferred cell suspension. Splenic T cells suppressing the induction of DH to HSV were characterized as being both Lyt 1+2- and Lyt 1-2+ 4 weeks after their induction. At earlier times, i.e., after 7 days, the suppression was mediated solely by the Lyt 1+2- population. Thereafter, a progressive increase in the contribution of the Lyt 1-2+ suppressor was observed. Both the early and later phases of suppression were due to I-J positive cells. The nature of the two suppressor cell types is discussed in relation to suppressor cell "cascades" and to the pathogenesis of herpes simplex virus infection.

Animals↗
PubMed1978

Investigation of a cutaneous delayed hypersensitivity response as a means of detecting Salmonella dublin infection in cattle.

Delayed hypersensitivity reactions developed 48 to 96 h after intradermal injection of killed Salmonella dublin in 25 of 28 cattle which had been inoculated intravenously, and in five of 10 cattle which had been inoculated orally with S dublin 24 to 493 days previously. Control animals showed no delayed hypersensitivity reactions. Persistence of infection in five of the intravenously inoculated and in four of the orally inoculated animals was confirmed by isolation of S dublin from the carcases at necropsy one week after skin testing. Failure to isolate the organism from the carcases of 21 animals which had reacted positively to the intradermal test did not eliminate the possibility of their being carriers of S dublin. Skin testing was concluded to be a reliable means of identifying animals which had been, and possibly still were, infected systemically with S dublin. However recovered animals might be falsely identified as infected. Repeated testing gave misleading results.

Administration, Oral↗
PubMed1987

Nifedipine-induced hyporeactivity in delayed hypersensitivity skin tests.

Four patients and three healthy volunteers were submitted to delayed hypersensitivity skin tests to candidin, tuberculin, streptokinase/streptodornase (SK/SD) and mumps antigen before and after a 1 week treatment with nifedipine 10 mg q. 8h. A decrease in the scores of induration and erythema was observed, especially in response to SK/SD antigen challenge. We conclude that nifedipine may induce an anergy status in delayed hypersensitivity skin tests.

Humans↗
PubMed1983

Delayed hypersensitivity in mast-cell-deficient mice.

The ability of mast cell-deficient Wf/Wf and W/Wv mice to produced delayed hypersensitivity responses was examined. The W/Wv mice did not have detectable mast cells and could not produce IgE-mediated passive cutaneous anaphylaxis. Mice of both genotypes produced large delayed hypersensitivity responses to the contact sensitizers oxazolone and picryl chloride. The responses were indistinguishable from responses of control mice when challenged with optimal or suboptimal doses of antigen. Delayed hypersensitivity could be transferred into Wf/Wf mice by an antigen-specific T cell line, and the proliferative responses in the lymph nodes of these mice after, painting with sensitizer, were normal.

Animals↗