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At least 19 recordsLinked to original sources
PubMed1979

Mechanisms of hypersensitivity: cellular interactions. Basophil arrival and function in tissue hypersensitivity reactions.

Bone marrow-derived blood basophils are recruited into the tissues by immuno mechanisms in a variety of delayed time-course hypersensitivity responses. In the skin these are called cutaneous basophil hypersensitivity (CBH) reactions. In guinea pigs, it is now established that the elicitation of CBH is dependent on T cell- and/or (antibody)-triggered mechanisms. Both are subject to modulation. T cell-mediated CBH seems to be suppressed in basophil-poor tuberculin-type reactions. B cells mediate CBH via antibody of IgG1 isotype through mechanisms that involve Fc receptors, which can be competitively blocked. After basophils arrive at a CBH reaction they can be triggered by antigen to immediately release mediators such as histamine. Thus, one consequence of the arrival and accumulation of basophils at delayed hypersensitivity reactions is to augment the anaphylactic potential of a given tissue site. In reactions to parasites, release of mediators by tissue basophils seems to aid in the expulsion of these multicellular organisms, In addition, histamine released by recruited basophils, or by locally resident mast cells, may modulate some delayed reactions through stimulation of histamine-2 receptors on cells such as T lymphocytes. In mice, mast cell release of serotonin and subsequent stimulation of the local vasculature seems to be required to allow diapedesis and tissue accumulation of various bone marrow-derived accessory leukocytes in delayed-type hypersensitivity responses. Thus, basophils and mast cells, and their release of mediators such as vasoactive amines, are involved in the onset, development, and function of various tissue hypersensitivity responses.

Anaphylaxis↗
PubMed1979

Interaction among IgE-mediated hypersensitivity reaction, PCA reaction and delayed hypersensitivity reaction (at local skin sites of monkeys).

The effect of the IgE-mediated reaction on the passive cutaneous anaphylaxis (PCA) reaction was studied at local skin sites of monkeys, and we found that the IgE-mediated reaction appeared to enhance the PCA reaction. Interactions among IgE-mediated reaction, PCA reaction and delayed hypersensitivity reaction were also determined. Contact dermatitis induced with DNCB was utilized as the delayed hypersensitivity reaction. The IgE-mediated reactior or PCA reaction, as well as simple serum irritation, enhanced the delayed hypersensitivity reaction. It is thus assumed that the IgE-mediated reaction enhances the PCA reaction and that this in turn accelerates the delayed hypersensitivity reaction.

Animals↗
PubMed1976

Delayed hypersensitivity to fungal antigens in mice. II. Molecular classes in immunogenic RNA extracts that transfer delayed hypersensitivity.

The transfer of delayed hypersensitivity to Coccidioides immitis and Candida albicans antigens with immunogenic RNA extracts was studied in a mouse model. Sensitivity was measured by skin tests and footpad swelling responses. Immunogenic RNA converted normal spleen cells in vitro so that they produced antigen-specific delayed hypersensitivity in mice that were given injections of the cells. RNase reduced the rate of, but did not abolish, in vitro interaction of immunogenic RNA extracts with lymphocytes. Immunogenic RNA transferred sensitivity on direct intraperitoneal inoculation into mice. The transfer ability was resistant to RNase preparations active against both single- and double-stranded RNA. Sedimentation gradient fractions of the immunogenic RNA were assayed by intraperitoneal injection, and converting activity was found in two fractions, greater than 33S and 6S-13S. After treatment with RNase, all activity was shifted to the less than 6S fraction. Two fractions of the immunogenic RNA in its native state (greater than 33S and 6S-13S) were also able to convert spleen cells. The data indicate that the transfer of delayed hypersensitivity by immunogenic RNA preparations is associated with RNA but may not require the intact RNA molecule.

Animals↗
PubMed1977

Relation between delayed skin reactivity and macrophage migration inhibition or lymphocyte transformation in tuberculin-type hypersensitivity and Jones-Mote hypersensitivity.

Precise time-course studies on delayed skin reaction, lymphocyte transformation and macrophage migration inhibition were carried out from day 3 to 270 and from day 3 to 120, respectively, in guinea pigs immunized with bovine gamma-globulin (BGG) in complete Freund's adjuvant (CFA) and those immunized with BGG in incomplete Freund's adjuvant (IFA). a) Delayed skin reactions could be elicited for a long period of time after immunization with BGG in CFA in the presence of prominent antibody production and were accompanied by induration. b) Delayed reactions could be elicited transiently after immunization with BGG in IFA and were not accompanied by induration. c) At the peak of hypersensitivity, infiltrating cells at the reaction sites were composed largely of mononuclear cells and basophils, respectively, in the animals immunized with BGG and CFA and those immunized with BGG in IFA. d) Uptake of 3H-thymidine by lymphocytes was increased remarkably in the presence of BGG when cells were obtained at early stages after immunization by both methods. e) Macrophage migration inhibition was strongly positive in animals immunized with BGG in CFA but weakly positive in those immunized with BGG in IFA. Increased lymphocyte transformation preceded the appearance of positive migration inhibition. f) After immunization with BGG in CFA, Jones-Mote hypersensitivity appeared to precede the development of tuberculin-type hypersensitivity.

Animals↗
PubMed1976

Relationships among differentiated T-cell subpopulations. I. Dissociated development of tuberculin type hypersensitivity, Jones-Mote type hypersensitivity and activation of helper function.

Relationships among tuberculin type hypersensitivity, Jones-Mote type hypersensitivity and activation of helper T cells were studied in AKR mice by means of footpad reaction, migration inhibition test and antibody production against the trinitrophenyl group. (1) Immunization with SRBC in saline, Freund's incomplete adjuvant (FIA) or complete adjuvant (FCA) and fixed-SRBC (FRBC) in FIA- or FCA-induced delayed hypersensitivity as demonstrated by footpad swelling. (2) Migration inhibition was positive in the groups immunized with SRBC or FRBC in FCA, but negative in those immunized with SRBC in saline or FIA or FRBC in FIA. This may suggest that the former has to be assigned to tuberculin type and the latter to Jones-Mote type. (3) Both pre-treatment with BCG and with cyclophosphamide (CY) augmented delayed footpad reaction in the mice immunized with SRBC in saline. However, migration inhibition was positive only in the group pre-treated with BCG. BCG may convert the reaction from Jones-Mote type to tuberculin type, while CY may augment the reaction of Jones-Mote type. (4) FRBC in saline scarcely induced delayed footpad reaction, whereas they activated helper function efficiently. Thus, three types of immunological phenomena attributable to the functions of T cells may depend upon distinct subpopulations of differentiated T cells which are raised by different methods of immunization.

Animals↗
PubMed1976

Chronic hypersensitivity lung disease with recurrent episodes of hypersensitivity pneumonitis due to a contaminated central humidifer.

A child with a 4-year history of acute and chronic respiratory symptoms of unknown aetiology was investigated for hypersensitivity pneumonitis. Lung disease due to inhalation of material from a contaminated central humidifier was suggested by the clinical history, the presence of precipitating antibodies in the serum against the humidifier water, a pulmonary response to challenge with the humidifier water, and marked improvement after removal of the humidifier. No fungi were cultured from the humidifier nor were antibodies against a number of fungal antigens identified by radioimmunoassay inhibition techniques. Antigenic material was found in the humidifier water and the household water prior to its reaching the humidifier. This antigenic material was not found in laboratory tap water supplied from the same general source (Lake Michigan) but from a different pumping station. Three of the child's siblings gave histories suggestive of a single concurrent episode of acute hypersensitivity pneumonitis and one sibling had a history suggestive of chronic hypersensitivity lung disease. No association could be found between HLA-haplotypy and disease in the patient and the siblings.

Alveolitis, Extrinsic Allergic↗
PubMed1977

Studies on delayed hypersensitivity in mice. I, Physicochemical and biological properties of preferential antigens for inducing delayed hypersensitivity in mice.

Variously modified protein antigens were tested by footpad assay to clarify the effect of these medications in producing delayed hypersensitivity in mice. The most potent antigen examined was carboxyl-methylated serum albumins. These antigens were highly basic proteins and hydrophobic compared with native serum proteins. They stimulate humoral antibody response in mice poorly, and remain at the subcutaneous injection site much longer than native serum albumins. In vitro tests of susceptibility of thymus and spleen cells and peritoneal macrophages to the antigens revealed that methylated serum albumins possessed the stimulatory activity to the latter and were toxic to the former. As for macrophage, fluorescein-labelled methylated serum albumin showed an affinity to their membrane and were phagocytosed, but FITC-BSA did not show any affinity to the macrophages. These biological activities to tissue or cells may be contributable to render methylated serum albumins to induce and elicit delayed hypersensitivity preferentially in mice.

Animals↗
PubMed1976

Studies on delayed-type hypersensitivity to hen egg-white lysozyme. I. Peptide fragments of lysozyme inducing delayed-type hypersensitivity.

Eleven peaks were separated by Carboxymethyl-cellulose column chromatography of peptic digest of lysozyme. Being stronger in antigenic activity two peaks of them, P-3 and P-9, were selected and purified further respectively by Amberlite IRC-50 and Sephadex G-50 column chromatography. As the results, PP-3 and PP-9 were obtained each as a single peak. For estimation of their capacities to induce delayed-type hypersensitivity, the antigen-induced 3H-thymidine incorporation, the migration inhibition of peritoneal cells and the delayed-type skin reaction were tested in guinea pigs immunized with native lysozyme or any of its fractions. PP-9 was almost as active as intact lysozyme in these capacities. On the other hand, PP-3 showed a slight inhibition of migration of peritoneal cells and no stimulation of 3H-thymidine incorporation into the lymph node cells. Moreover, the delayed-type skin reaction elicited by PP-3 was always weaker than that elicited by PP-9. Guinea pigs immunized with either PP-3 or PP-9 were also tested for these reactions. PP-9 and native lysozyme elicited these reactions in guinea pigs immunized with PP-9, but PP-3 did not. On the other hand, PP-3 and lysozyme elicited these reactions in those immunized with PP-3, but PP-9 did not. The possibility of recognition of two functionally different areas, one for production of the circulating antibody and the other for induction of delayed-type hypersensitivity, on the lysozyme molecule was discussed.

Animals↗
PubMed1979

An animal model of hypersensitivity pneumonitis in rabbits. Development of chronic pulmonary inflammation and cell-mediated hypersensitivity after repeated aerosol challenge.

Chronic pulmonary inflammation was produced in immunized rabbits by repeated aerosol exposure to soluble antigen. The pulmonary inflammatory response was correlated with the development of cell-mediated hypersensitivity in the lung as evaluated by migration-inhibition studies using bronchoalveolar cells. Such inflammation could be produced with either pigeon dropping extract, an etiologic agent of hypersensitivity pneumonitis, or with human gamma globulin. Development of the inflammatory response was immunospecific and could not be transferred to normal recipients with large quantities of immune serum. Collectively, these data suggest that the development of pulmonary inflammation was due to a cell-mediated immunologic reaction in the lung.

Aerosols↗
PubMed1977

Regulation of delayed-type hypersensitivity. I. T suppressor cells for delayed-type hypersensitivity to sheep erythrocytes in mice.

Mice injected with 1 X 10(8) sheep red blood cells (SRBC) into the footpad showed high levels of delayed-type hypersensitivity (DTH) to SRBC 4-8 days after the injection. In contrast, mice injected intravenously with 1 X 10(9) SRBC were unresponsive to DTH induction through 1 X 10(8) SRBC injected into the footpad. This suppression of DTH was maintained for at least 6 weeks and was transferable spleen, lymph node and thymus cells to normal syngeneic recipients. Bone marrow cells, on the other hand, did not contain the suppressor cells. The suppression of DTH was antigen-specific in that DTH to chicken red blood cells and contact sensitivity to 2,4-dinitrofluorobenzene was not affected. The suppressor cells were theta-positive and Ig-negative. They appeared in the spleen in optimum number 3-4 days after induction. The suppressor cells affected both the induction and manifestation of DTH. The presence of suppressor and effector cells for DTH inducible by different routes of antigenic presentation reflects the dynamic balance in the regulation of DTH.

Animals↗
PubMed1978

Regulation of delayed-type hypersensitivity. II. Specific suppressor factor for delayed-type hypersensitivity to sheep erythrocytes in mice.

An antigen-specific suppressor factor for delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) in mice is described. Lymph node cells and spleen cells from mice injected intravenously with 1 x 10(9) SRBC 4 days previously were incubated in vitro for 48 h in culture medium. Supernatant obtained from the culture inhibited the induction of DTH to SRBC in normal mice. It also suppressed the expression of DTH in presensitized mice. The suppression is specific as the suppressor factor had no effect on the DTH to noncross-reacting antigen, chicken red blood cells. Treatment of the spleen cells with anti-theta serum and complement prevented the production of the suppressor factor, whereas treatment with anti-Ig serum and complement had no effect. Suppressor factor produced by H-2k mice suppressed the DTH in H-2b mice. The factor thus seems to act across the H-2 barrier. The suppressor factor was not removed by adsorption with goat anti-mouse immunoglobulin immunoadsorbent, but could be adsorbed by SRBC. It was stable at 56 degrees C for 1 h, but was partially inactivated by freezing and thawing. The factor has a molecular weight of less than 35 000 daltons.

Animals↗
PubMed1978

Regulation of delayed-type hypersensitivity. III. Effect of cyclophosphamide on the suppressor cells for delayed-type hypersensitivity to sheep erythrocytes in mice.

A previous study (Eur. J. Immunol. 1977. 7: 714) has shown that mice injected intravenously (i.v.) with 4 x10(9) sheep red blood cells (SRBC) produce cells which suppress delayed-type hypersensitivity (DTH). These suppressor cells are theta-positive, antigen-specific and act via a soluble factor which does not bear immunoglobulin determinants (Eur. J. Immunol. 1978. 8: 168). The present paper demonstrates that these suppressor cells are inhibitable by cyclophosphamide (CY). Mice injected with graded amounts of CY two days prior to SRBC injection, showed maximum augmentation of DTH at 200 mg/kg body weight, a dose which completely suppressed the appearance of splenic plaque-forming cells (PFC) to SRBC. In contrast, lower doses of CY enhanced both DTH and PFC responses. Time course studies showed that CY inhibited the precursors of suppressor cells and had little or no effect on suppressor cells which have already encountered antigens. This was further confirmed by passive transfer studies which showed tha- suppressor cells were inhibited if CY was administered at the same time or 2 days before SRBC injection, but were not affected if CY was given after antigen stimulation. Direct evidence for the effect of CY on suppressor cells was obtained by cell fractination with a Ficoll density gradient. The denser suppressor cell population was absent from the spleens of mice treated with 200 mg/kg of CY 2 days before i.v. injection with 1 x 10(9) SRBC.

Animals↗
PubMed1979

Regulation of delayed-type hypersensitivity IV. Antigen-specific suppressor cells for delayed-type hypersensitivity induced by lipopolysaccharide and sheep erythrocytes in mice.

Mice injected subcutaneously with 1 x 10(8) sheep red blood cells (SRBC) developed high levels of delayed-type hypersensitivity (DTH) to SRBC 4-8 days after injection. Such DTH was suppressed when 100 microgram lipopolysaccharide (LPS) was injected intravenously 1-2 days before or at the time of SRBC injection. This suppression of DTH was transferable by spleen, lymph node, thymus and bone marrow cells to sensitized or normal syngeneic recipients, but could not be transferred by serum. Suppressor cells were not induced by LPS alone or SRBC alone, and they were antigen-specific since DTH to chicken red blood cells was not affected. The suppressor cells appeared in the spleen in optimum number 3-4 days after induction. They were theta-negative and Ig-positive as judged by antiserum plus complement treatment and by Ig rosette separation. Attempts to obtain soluble suppressor factor from the suppressor cells by sonication or in vitro incubation were unsuccessful. Mitomycin C treatment of the suppressor cells completely abolished the suppressor activity. Thus, LPS, in conjunction with antigen, appears to induce a population of specific suppressor B cells which are capable of regulating T cell function.

Animals↗
PubMed1977

Studies on delayed hypersensitivity in mice. III. Evidence for suppressive regulatory T1-cell population in delayed hypersensitivity.

T-T-cell interactions involved in delayed hypersensitivity (DH) response have been studied by employing delayed foot pad assay to methylated human serum albumin in C57BL/6J mice. The DH response, one of the T-cell manifestations of cell-mediated immune response is suppressively regulated by T cells and such observation was based on studies of age-associated kinetics of foot pad reaction and effects of cell transfer and adult thymectomy on developing DH response. These suppressively regulatory T cells in DH have a life span of less than 4 wk and a constant derivation from the thymus is required. Such cells are numerous in the young mouse thymus and few in the spleen and thymus of old mice. On the one hand, the presence of a long-lived effector T-cell population was suggested in DH. These cells are numerous in the spleen and are low responders to phytohemagglutinin in vitro. It is assumed that these suppressive T cells interact with antigen-reactive cells at their proliferating stage by recognition of the iodiotypic difference through surface receptors. As in the case of graft-vs.-host and humoral response in vivo, three different subsets of immune competent cells participate in the DH response. These cells consist of one specifically antigen-reactive T cell, one suppressive regulatory T cell, and one bone marrow-derived cell, a macrophage that responds to a chemical mediator from sensitized effector T cells and that develops a DH skin lesion nonspecifically.

Aging↗
PubMed1978

Studies on delayed hypersensitivity to protein antigen. Induction of delayed hypersensitivity by chemically modified antigen.

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.

Amylases↗
PubMed1978

Delayed hypersensitivity in mice induced by intravenous sensitization with sheep erythrocytes: evidence for tuberculin type delayed hypersensitivity of the reaction.

Delayed hypersensitivity (DH) reaction can be induced in mice by intravenous sensitization with sheep erythrocytes (SRBC). However, as the sensitizing procedure is quite different from a usual mode of sensitization for DH using complete Freund's adjuvant (FCA), the nature of this reaction has been a matter of controversy. In an attempt to characterize this reaction, we placed special interest on two possibilities regarding the nature of this reaction; Jones-Mote reaction or tuberculin type DH. From the kinetics study on the DH after challenge, the DH reaction to SRBC in mice by intravenous sensitization was clearly distinguished from the Arthus reaction. The dose-response pattern of this reaction also suggested that the contribution of Arthus reactivity to delayed reactivity was negligible. Cell reconstitution experiments revealed this DH to be quantitatively thymus cell dependent. Furthermore, this DH required macrophages at its manifestation stage, and appearance of basophil infiltration at the lesion was absent. In addition, strain difference and ageing of host mice influenced the DH reaction in exactly the same fashion in which these factors influence the tuberculin type-DH induced by subcutaneous sensitization with methylated human serum albumin (MHSA) in FCA. Taken collectively, it was concluded that this DH reaction can be categorized as the tuberculin type.

Aging↗