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Delayed hypersensitivity in guinea pigs was produced by immunization. with a conjugate prepared by coupling diazotized arsanilic acid to polytyrosine. The resulting sensitivity could be demonstrated by skin test with conjugates prepared from a wide variety of tyrosine-containing proteins. Definite but smaller degrees of sensitivity could be induced with conjugates of proteins containing little or no tyrosine. The apparent absence of carrier-specificity is considered to be due to the narrowed range of immunologic response produced by immunization with polytyrosine-azobenzenearsonate. Injections of the hapten N-acetyltyrosine-azobenzenearsonate was found to suppress completely the delayed reaction attributable to the tyrosine-azobenzenearsonate group. The same hapten was only slightly effective in suppressing reactions in guinea pigs immunized with guinea pig serum albumin-azobenzenearsonate, suggesting that a broader range of specificities is involved with such antigens. Confirmation of such increased range of specificity attributable to antigenic determinants contributed by the carrier protein was obtained by desensitization studies with N-acetyltyrosine-azobenzenearsonate and guinea pig serum albumin-azobenzoate. While separately these materials produced only a slight decrease in skin reactivity to guinea pig serum albumin-azobenzenearsonate, the combination was found to give almost complete suppression.
To detect cell immunity characterized by delayed postvaccination hypersensitivity to anthrax in man and assess its dynamics, vaccination using unencapsulated live anthrax vaccine was performed in 668 healthy volunteers. Vaccination was performed either by scarification (n = 172), subcutaneous injection (n = 202), or low-dose (n = 202) or high-dose (n = 83) inhalation. The anthraxin intradermal tests were performed in each patient at various times during the year following vaccination (D7, D15, D90, D180, D365). This study confirm that, regardless of the mode of administration, the vaccine induces cell-mediated immunity in man, as determined by positive anthraxine skin test. The incidence of positive tests decreases with time regardless of the mode of vaccination. After one year, the test remained positive in 34.8% of subjects vaccinated by subcutaneous injection, 37.5% vaccinated by low-dose inhalation, 34.2% vaccinated by high-dose inhalation, and 22.4% vaccinated by scarification. These findings are in agreement with those obtained in clinical epidemiological studies documenting the effectiveness of encapsulated live anthrax vaccine in man.
Delayed hypersensitivity was produced in donor Lewis rats by sensitization with soluble protein antigens emulsified in complete Freund's adjuvant. Cells of their thoracic duct lymph were collected for varying periods of time and transferred intravenously to isogenic Lewis recipients. With this model the following conclusions were reached: 1. Delayed hypersensitivity was transferred by thoracic duct cells. 2. The longer the drainage of the thoracic duct, the fewer cells were needed to achieve a successful transfer. With continuing drainage the proportion of small lymphocytes decreased and large cells increased. There was, therefore, a better correlation between successful transfer of delayed hypersensitivity and the number of large cells transfused than between positive skin reactions and transfer of small lymphocytes. 3. Prolonged fistula of the thoracic duct did not diminish the skin reaction of sensitized donors to specific antigen. 4. Delayed hypersensitivity was elicited in recipients 3 wk after transfer of sensitized cells. There was evidence that delayed hypersensitivity was enhanced in recipients, possibly because of prior skin testing. 5. Total body X-irradiation abolished the lesions of passively transferred delayed hypersensitivity. Recovery of positive skin tests was observed 19 to 20 days later. 6. The lesions of delayed hypersensitivity were probably mediated by cells. There was no evidence that a circulating high affinity antibody played a role in this type of immunologic reaction.
Delayed hypersensitivity reactions to a battery of antigens were measured in 145 Tunisian breast cancer patients to determine whether an immunologic mechanism could be detected which might explain the high frequency (60%) of the rapidly progressing form in Tunisian breast cancer patients. Although a greater proportion (30%) of patients with rapily progressing breast cancer reacted to extracts of a breast tumor antigen (2937) than patients without PEV (9%), no significnat difference between PEV and non-PEV patients could be found in reactivity to DNCB, standard microbial antigens, or extracts from tissue culture cell lines. Rapidly progressing breast cancer in Tunisia is not associated with an impairment of delayed hypersensitivity.
Delayed hypersensitivity to four common antigens was assessed in 32 patients undergoing major abdominal surgery randomly allocated to either general anesthesia (fentanyl + O2/N2O + postoperative pain relief with systemic opiates) or general anaesthesia + epidural analgesia (local anaesthetics + morphine) continued for 72 h. Skin-test responses were performed 2 days before surgery and 1 day after surgery and compared to a similar retesting schedule in 16 comparable non-operative control patients. Cumulated mean skin-test responses increased from 1290 to 2330 mm2 (P less than 0.0001) during retesting in the non-operative control group. In contrast, mean skin-test responses in patients operated during general anaesthesia + systemic opiates for postoperative pain relief fell from 1422 to 1227 mm2 (P = 0.3) and in patients receiving epidural analgesia from 1228 to 890 mm2 (P = 0.06), without statistically significant differences between these two groups (P greater than 0.5). Thus, surgery leads to depression of delayed hypersensitivity and this impairment in immunofunction is not modified by an epidural analgesic regimen providing adequate pain relief.
Delayed hypersensitivity was assessed with four antigens, viz. purified protein derivative of tuberculin (PPD), Candida albicans, streptokinase/streptodornase and mumps, 48 hours before and 24 hours after elective major abdominal surgery in 24 patients. Cumulated areas of skin response were recorded on the basis of readings 24 and 48 hours after antigen stimulation. A control group of 16 patients was similarly assessed, but without surgery between the two test occasions. Retesting in this control group increased the cumulated skin response area in all patients. The respective means for the two tests were 1 290 +/- 222 to 2 330 +/- 365 mm2 (p less than 0.0001), demonstrating a pronounced booster action by the initial test. In contrast, the surgical patients showed a decrease, from 1 559 +/- 203 preoperatively to 1 230 +/- 210 mm2 postoperatively (p = 0.14). The postoperative response was significantly lower than the retesting response in the controls without surgery (p = 0.02), indicating that surgery leads to depression of delayed hypersensitivity response. The preoperative cumulated skin test response correlated with age (r = -0.66, p less than 0.001) and with serum albumin (r = 0.59, p less than 0.01). Postoperative depression of the skin test response also was related to age (r = 0.53, p less than 0.01) and with postoperative fall in s-albumin (r = 0.51, p less than 0.05). The results emphasize that interpretation of serial skin testing in surgical patients is not adequate unless comparison is made with a similar retesting regimen in nonsurgical patients.
Delayed skin reactions or peritoneal cell migration inhibition were elicited in guinea-pigs or rats with egg albumin, diphtheria toxoid, or tuberculin-purified protein derivative either separately or with various combinations of two antigens. When the skin reactions or migration inhibition with the component antigens alone were relatively strong, the corresponding combination elicited weaker reactions than calculated assuming that the antigens would add upon each other independently, i.e. the non-specific phase was limiting the manifestation. When the reactivity to both components was undetectable or very weak, the combination elicited stronger reactions than calculated, implying synergism of antigen recognition. The combinations of two weakly positive or intermediate reactivities were close to the calculated values in both the diameter of erythema, skin thickness and migration percentage. These results may help in assessing the biological significance of findings in delayed hypersensitivity: even minor differences in strong manifestations may mean great differences in terms of specific lymphocytes, while marginal changes of antigen recognition may lead to apparently great changes of manifestation, when very weak reactivities are measured.
Ear/footpad swelling following sensitization and challenge with 2,4-dinitrofluorobenzene (DNFB)/allogenic splenocytes (AS) were used to monitor the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on contact hypersensitivity (CHS) and delayed hypersensitivity (DHS) reactions, respectively. Topical treatment of dorsal or ventral SENCAR mouse skin 4x with 2 micrograms of TPA prior to sensitization of dorsal skin with DNFB suppressed attempts to induce CHS by subsequent challenge with DNFB. The adoptive transfer of splenocytes isolated from mice pretreated on the dorsum with TPA prior to dorsal sensitization with DNFB inhibited the development of CHS to DNFB in recipient mice. Conversely, topical treatment with TPA prior to s.c. sensitization with AS neither suppressed subsequent attempts to induce DHS, nor resulted in the generation of a splenocyte population capable of suppressing DHS reactions in adoptive transfer studies. Thus, promoting doses of topically applied TPA has differential effects on CHS and DHS reactions.
Two potential mechanisms for terminating delayed hypersensitivity (DH) reactions have been examined in desensitized guinea pigs. Lack of macrophage responsiveness to lymphokines was sought as an explanation for the reduced ability of these animals to express delayed hypersensitivity. Skin-reactive factor was injected into the skin of desensitized guinea pigs and a control group of similarly immunized animals. The resulting inflammatory reactions were similar in size and intensity in both groups indicating normal macrophage responsiveness in the desensitized state. Passive cellular transfer of DH responses to desensitized animals was markedly less successful than transfer to normal animals. However, cells from desensitized guinea pigs did transfer DH responsiveness to normal animals. These data support the concept of a humoral suppressant of cellular immunity, perhaps acting as a feedback inhibitor, produced when guinea pigs are desensitized.
Guinea pigs experimentally infected with mumps virus develop a delayed, hypersensitive skin reaction following the intradermal injection of heat-inactivated mumps virus. This in vivo hypersensitivity is accompanied by a state of cellular hypersensitivity which can be demonstrated in vitro by the addition of mumps viral antigen to cultures of splenic macrophages, following which they become less motile and undergo lysis. These observations support the hypothesis that the state of hypersensitivity which develops early in mumps virus infections may have a role in the pathogenesis of the disease.
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it was shown in our previous paper that mice primed with chemically modified bacterial alpha-amylase (BaA), which was neither cross-reactive with anti-BaA antibody nor able to induce a humoral anti-BaA response, developed enhanced responses to a subsequent challenge with native BaA and that the magnitude of the immunological memory was closely related to the priming dose of modified BaA. This paper describes the experimental conditions for induction of delayed hypersensitivity (DH) by modified BaA in relation to the development of immunological memory for antibody response to native BaA. Mice primed with either an intraperitoneal (i.p.) or subcutaneous (s.c.) injection of modified BaA in complete Freunds adjuvant (CFA) developed enhanced anti-BaA as the immunogen and modified BaA as the eliciting antigen, the relationship of anti-BaA responses to a subsequent challenge with BaA. In contrast, when mice were immunized with an s.c. injection of the modified BaA only, a significant level of DH to native BaA could be induced, as measured by the footpad reaction (FPR). The highest degree of DH was observed in mice given 50 micrograms of modified BaA. DH was detectable within 5 days and persisted for 25 days after immunization. In the reciprocal combination of native BaA as the immunogen and modified BaA as the eliciting antigen, the relationship of anti-BaA responses to DH was examined. The primary anti-BaA responses induced by an i.p. injection of large doses of BaA was markedly higher than those induced by an s.c. injection, while DH was exhibited only in mice given s.c. injection of BaA in CFA. With respect to DH to native BaA induced by the modified BaA, it was shown that C3H/He mice were high and C57BL/6 mice were low responders.
Injections of various conjugates of arsanilic acid into newborn guinea pigs produced a specific tolerance in respect to subsequent development of hapten-specific delayed hypersensitivity. In general, larger polyvalent conjugates produced longer lasting and more profound suppression of delayed sensitivity than did the smaller ones. Carrier injections alone were ineffective. At lower doses of conjugate, breakthrough of tolerance occurred first with animals immunized with the heterologous carrier conjugate. The duration of tolerance produced by injection of monovalent conjugates into neonates is in contrast to the transient inhibition produced by the same conjugates in previously sensitized animals, suggesting that different target cells may be involved in these two phenomena.
The delayed skin-test response to four antigens was assessed before and after 6 weeks' cimetidine therapy in patients with duodenal-ulcer disease. In the eight patients who received cimetidine there was a significant increase in both erythema and induration after six weeks' cimetidine therapy. In contrast, the intensity of delayed-hypersensitivity reactions at 6 weeks was not increased in eight control patients who did not receive cimetidine. These studies indicate that therapy with an H2-receptor antagonist may be associated with an augmentation of delayed hypersensitivity responses.