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PubMed1955

Studies on hypersensitivity of human tissues in vitro. I. Tuberculin hypersensitivity.

A new simple method of evaluating specific cytotoxicity to tuberculoprotein in the study of tuberculin hypersensitivity in vitro by comparing cell populations is presented. Utilizing this technic it was possible to reproduce Rich's results (1, 2) using human tissues of reticuloendothelial origin. The demonstration of the specific cytotoxic phenomenon in tuberculin-sensitive human tissues indicates that the principle elaborated by Rich (2) of specific changes in the individual fixed tissue cells in tuberculin hypersensitivity, possibly related to cellular antibodies, applies to human subjects as well as to the animals heretofore studied. Preliminary observations suggest that macrophages from donors with clinically active tuberculosis are more sensitive to tuberculoprotein than macrophages from tuberculin-positive donors without clinically active disease. Macrophages from tuberculin-positive donors appeared to be more sensitive to tuberculoprotein than fibroblasts derived from the same tissue. An inhibition of cell proliferation was seen when both cell types were exposed to PPD. In addition macrophages responded to tuberculoprotein with gross morphological changes and eventual cytolysis.

Animals↗
PubMed1973

Regulation of delayed hypersensitivity. Failure to transfer delayed hypersensitivity to desensitized guinea pigs.

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.

Animals↗
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↗
PubMed1981

Immediate hypersensitivity in the guinea pig conjunctiva. III. long-term persistence of the hypersensitive state and characterization of antibodies.

The ocular immediate hypersensitivity reaction in guinea pigs to topically applied normal rabbit serum can be evoked as long as 4 years after sensitization. The reaction was as severe and tended to persist for longer than that evoked 6 months after sensitization. Passive cutaneous anaphylaxis tests showed that very high titres of homocytotropic antibodies were present and that both IgE- and IgG1-like antibodies were involved. Sensitization with one set of injections instead of two was not consistently successful and the response on challenge was mild to moderate. Pretreatment of eyes with Isoptocarpine before antigenic challenge had no effect on the response. The addition of bacterial lipopolysaccharide to the first set of sensitizing injections produced hypersensitivity in animals which were otherwise refractory to sensitization.

Animals↗
PubMed2001

CCR6-deficient mice have impaired leukocyte homeostasis and altered contact hypersensitivity and delayed-type hypersensitivity responses.

CCR6 expression in dendritic, T, and B cells suggests that this beta-chemokine receptor may regulate the migration and recruitment of antigen-presenting and immunocompetent cells during inflammatory and immunological responses. Here we demonstrate that CCR6-/- mice have underdeveloped Peyer's patches, in which the myeloid CD11b+ CD11c+ dendritic-cell subset is not present in the subepithelial dome. CCR6-/- mice also have increased numbers in T-cell subpopulations within the intestinal mucosa. In 2,4-dinitrofluorobenzene-induced contact hypersensitivity (CHS) studies, CCR6-/- mice developed more severe and more persistent inflammation than wild-type (WT) animals. Conversely, in a delayed-type hypersensitivity (DTH) model induced with allogeneic splenocytes, CCR6-/- mice developed no inflammatory response. The altered responses seen in the CHS and DTH assays suggest the existence of a defect in the activation and/or migration of the CD4(+) T-cell subsets that downregulate or elicit the inflammation response, respectively. These findings underscore the role of CCR6 in cutaneous and intestinal immunity and the utility of CCR6-/- mice as a model to study pathologies in these tissues. This article was published online in advance of the print edition. The date of publication is available from the JCI website, http://www.jci.org.

Animals↗
PubMed1993

Differential modulation of contact hypersensitivity and delayed hypersensitivity reactions by topical application of 12-O-tetradecanoylphorbol-13-acetate.

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.

Administration, Topical↗
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↗
PubMed2000

Retinal pigment epithelial hypersensitivity, an association with vision loss: RPE hypersensitivity complicating paraneoplastic retinopathies.

PURPOSE: Paraneoplastic retinopathies are currently identified and classified according to specific anti-retina antibody reactions. These cancer-induced retinal degenerations can be accompanied by changes in the character of the retinal pigment epithelium (RPE) indicative of additional, and superimposed, pathologic activity. The antibody reactions of 11 paraneoplastic retinopathy patients were evaluated to identify those whose immunologic abnormalities included indications of RPE hypersensitivity. The pathologic significance of this anomaly was evaluated upon viable monolayers of RPE, in the presence and absence of complement. METHODS: Comparisons of antibody reactions were made using: (1) indirect immunohistochemistry on sections of rhesus monkey eyes; (2) Western blot reactions on extracts of rhesus monkey retina and in vitro-propagated rhesus RPE; and (3) an evaluation of antibody influence upon the metabolic activity of viable monolayers of rhesus RPE cells. RESULTS: Indirect immunohistochemistry on sections of monkey eyes identified antibodies reactive with RPE in four of the 11 cancer patients. The same four were found to identify a 57 kd protein component of these cells in Western blot reactions of RPE and to inhibit the metabolic activity of viable RPE cells through actions enhanced by the addition of complement. One subject from the reference comparison control group, a cancer-free patient with age-related macular degeneration, also exhibited comparable antibody activity with RPE. CONCLUSIONS: RPE hypersensitivity can present as a superimposed immunologic complication to the retinal degenerations of paraneoplastic retinopathies and those unrelated to malignancies. When activated, humoral aspects of the immune response are able to impart pathologic effects that inhibit RPE homeostasis and, consequently, the essential supportive functions of these cells. Since this immunologic abnormality is not confined to cancer patients, it should be considered potentially harmful when encountered in association with any type of vision loss.

Animals↗
PubMed1976

Cutaneous basophil hypersensitivity uncovered in the cell transfer of classical tuberculin hypersensitivity.

Cellular transfer of cutaneous basophil hypersensitivity (CBH) was studied. Guinea pigs immunized for CBH with incomplete Freund's adjuvant (IFA) provided cells which could transfer delayed and basophil-rich reactions in skin tests of recipients. Guinea pigs immunized with complete classical tuberculin-type delayed hypersensitivity reactions (DH), which are characteristically devoid of basophils. However, recipients of cells from donors with DH, surprisingly, were found to have delayed skin reactions containing large basophil infiltrates which were lacking in the donors. Thus, recipients of classical cell transfers of tuberculin-type DH had delayed reactions which resembled CBH. Control experiments verified that the cell transfer of CBH from donors with DH was due to passive transfer with live cells and not transfer of contaminating humoral factors or active sensitization of recipients. It was concluded that cutaneous basophil responses were suppressed in CFA-immunized donors and expressed in cell transfer recipients. Cells from donors immunized with CFA were enriched for nonadherent and nonimmunoglobulin-bearing lymphocytes by passage through nylon wool columns, and these cells transferred conjugate specific CBH reactions. It was concluded that cells mediating these transfers were probably T cells. The finding of basophils in cell transfers of DH and a variety of other findings suggesting complex regulation of basophil numbers in tissue lead to the conclusion that the term CBH be used to simply describe a basophil-containing skin reaction.

Animals↗
PubMed1991

Delayed-type hypersensitivity initiation by early-acting cells that are antigen mismatched or MHC incompatible with late-acting, delayed-type hypersensitivity effector T cells.

The elicitation of delayed-type hypersensitivity (DTH) responses in mice is mediated by the sequential activities of two different Ag-specific, Thy-1+ cells. A required early phase of elicitation is due to DTH-initiating Thy-1+ cells that are CD3- and sIg- and produce Ag-specific factors that act like IgE antibodies in that they sensitize the tissues, so that after local challenge with Ag there is release of the vasoactive amine serotonin. Released serotonin locally recruits and activates CD4+ Th-1 classical DTH effector T cells that secrete lymphokines that attract and activate a nonspecific perivascular infiltrate of circulating, bone marrow-derived leukocytes. The current study used isolated subpopulations of DTH-initiating and DTH-effector T cells to determine whether the two phases of the elicitation of DTH were entirely separate. The contact sensitivity model of DTH was used. Early-acting DTH-initiating cells, and late-acting DTH-effector T cells were either from oxazolone (OX)-immune or picryl chloride (PCl)-immune CBA or BALB/c donors and were transferred to CBA or BALB/c recipients. The results showed that DTH-initiation could be mediated by polyclonal DTH-initiating cells that were Ag mismatched or MHC incompatible with late-acting DTH effector T cells. In fact DTH-initiating cells could be both Ag mismatched and MHC incompatible with late-acting T cells. In addition, potential interactions between different cell populations were ruled out by showing that DTH-initiation could be mediated by a DTH-initiating clone that was Ag or MHC mismatched with the late-acting DTH-effector T cells. Thus, the OX-specific BALB/c clone could initiate DTH for PCl-specific CBA cells in CBA recipients if the recipients were challenged with both OX and PCl, but not when they were challenged with OX or PCl alone. We suggest, at least for the elicitation of DTH reactions in mice, that a more comprehensive description of these responses should accommodate the fact that there are early and late phase responses that each begin with Ag specificity and end with non-specific humoral factors. Inasmuch as the two Thy-1+ cells of DTH can be of different Ag specificity, this suggests that some forms of delayed and chronic inflammation, might be initiated by an immediate hypersensitivity-like immune reactivity to one set of Ag, and could be prolonged and perpetuated by delayed reactivity to another set of Ag.

Animals↗
PubMed1987

Anti-T cell monoclonal antibodies in vivo. I. Inhibition of delayed hypersensitivity but not cutaneous basophil hypersensitivity reactions.

As part of a study of the therapeutic potential of anti-T cell monoclonal antibodies, we studied the biologic effects of 8BE6, a mouse anti-guinea pig (GP) pan-T cell monoclonal antibody, on blood and tissue T cells and on the prototypic T cell-mediated reactions, classic delayed hypersensitivity (DH) and cutaneous basophil hypersensitivity (CBH). 8BE6 reacts to a 68,000 m.w. protein probably homologous with human CD5 (T1) and murine Lyt-1. A single dose of 1.8 to 3.4 mg 8BE6 caused lymphopenia and greater than 90% depletion of 8BE6+ peripheral T cells 1 to 72 hr later, and a significant but lesser decrease of lymphocytes reacting with another pan-T cell monoclonal antibody (p less than 0.02 at 24 hr). Free serum 8BE6 was detected for up to 48 hr after administration. Immunoperoxidase stains of tissue revealed that lymphocytes in lymph nodes and spleen were coated with mouse immunoglobulin 1 hr after antibody treatment and displayed in situ capping. Subsequently, there was a loss of T cells in all tissues (spleen, lymph node, liver, and kidney) except the thymus, with normal 8BE6 antigen staining returning by 72 hr. Areas of induration of DH reactions to PPD were reduced in 8BE6-treated GP, compared with pretreatment reactions in the same GP or in control-treated GP (p less than 0.001 for both). The numbers of infiltrating T cells and fibronectin-receptor-positive macrophages were also reduced. In contrast, 8BE6 had no effect on CBH reactions, as judged by erythema and basophil counts in 1-micron sections, although fewer T cells were found in reaction sites. There were no differences in IgM, fibronectin, or Ia staining between 8BE6-treated GP and controls. In vivo administration of a single dose of anti-T cell monoclonal antibody results in a transient, highly specific depletion of T cell populations in peripheral blood and tissues except the thymus. This treatment inhibits DH but not CBH reactions by systemic and local depletion of T cells.

Animals↗
PubMed1981

Delayed hypersensitivity to Staphylococcus aureus in mice: characterization of a membrane immunogen involved in delayed hypersensitivity.

Staphylococcal membrance proteins are potent initiators of delayed hypersensitivity following multiple subcutaneous injections of viable organisms. When the membranes are separated by exclusion chromatography they separate into three distinct fractions, one of which was responsible for the elicitation of footpad (FP) reactivity in sensitized mice. The active immunogen was characterized as a glycoprotein having a molecular weight of approximately 15,600 Daltons, with the peptide and carbohydrate moieties linked by covalent bonding. In vitro spleen cell stimulation and macrophage migration inhibition studies revealed that the active FP fraction was also the immunogen involved in these responses. The immunogenic fraction also had mitogenic properties as evidenced by the stimulation of non-sensitized spleen cells. These data characterize a glycoprotein present in Staphylococcus aureus cell membrane which is both immunogenic and mitogenic and is the principal immunogen responsible for the early delayed hypersensitivity response.

Animals↗
PubMed2005

Expression of the hypersensitive response-assisting protein in Arabidopsis results in harpin-dependent hypersensitive cell death in response to Erwinia carotovora.

Active defense mechanisms of plants against pathogens often include a rapid plant cell death known as the hypersensitive cell death (HCD). Hypersensitive response-assisting protein (HRAP) isolated from sweet pepper intensifies the harpin(Pss)-mediated HCD. Here we demonstrate that constitutive expression of the hrap gene in Arabidopsis results in an enhanced disease resistance towards soft rot pathogen, E. carotovora subsp. carotovora. This resistance was due to the induction of HCD since different HCD markers viz. Athsr3, Athsr4, ion leakage, H(2)O(2) and protein kinase were induced. One of the elicitor harpin proteins, HrpN, from Erwinia carotovora subsp. carotovora was able to induce a stronger HCD in hrap-Arabidopsis than non-transgenic controls. To elucidate the role of HrpN, we used E. carotovora subsp. carotovora defective in HrpN production. The hrpN(-) mutant did not induce disease resistance or HCD markers in hrap-Arabidopsis. These results imply that the disease resistance of hrap-Arabidopsis against a virulent pathogen is harpin dependent.

Arabidopsis↗
PubMed1985

Heparin-treated, v-myc-transformed chicken heart mesenchymal cells assume a normal morphology but are hypersensitive to epidermal growth factor (EGF) and brain fibroblast growth factor (bFGF); cells transformed by the v-Ha-ras oncogene are refractory to EGF and bFGF but are hypersensitive to insulin-like growth factors.

Chicken heart mesenchymal cells do not proliferate in culture medium containing heat-defibrinogenated plasma but proliferate briskly when incubated with epidermal growth factor (EGF) or brain fibroblast growth factor (bFGF) plus insulin-like growth factors (IGFs) or when infected with sarcoma or erythroblastosis viruses. When infected with the retrovirus MC29, which bears a v-myc oncogene, chicken heart mesenchymal cells proliferate at a more modest rate and become morphologically transformed. Heparin at 25 microgram/ml causes these MC29-transformed cells to become proliferatively quiescent and to assume a normal morphology. Heparin-treated MC29-infected cells are, however, 100 times more sensitive to EGF than are their normal, uninfected counterparts. MC29-infected cells appear, likewise, to be hypersensitive to bFGF and to PDGF preparations but not to insulin. We hypothesize, therefore, (i) that heparin prevents the generation by cells of a mitogen from plasma protein precursors in the culture medium; (ii) that the v-myc oncogene renders cells hypersensitive to EGF, bFGF, PDGF, and the putative plasma-protein-derived mitogen; and (iii) that MC29-infected cells must proliferate in order to manifest the transformed morphology. Chicken heart mesenchymal cells infected with a recombinant spleen necrosis virus containing a v-ras oncogene are morphologically transformed but proliferate only sluggishly in plasma-containing medium without added mitogenic hormones. Heparin does not significantly affect their behavior. They are refractory to mitogenic stimulation by EGF or bFGF suggesting that ras proteins mediate the effects of receptors for these hormones. The SNV/v-ras-infected cells proliferate briskly, however, in response to hyperphysiological concentrations of insulin, an IGF surrogate, and are considerably more sensitive to this IGF mitogenicity than are their normal, uninfected counterparts.

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↗
PubMed1994

[Hypersensitivity pneumonitis--histopathology of summer-type hypersensitivity pneumonitis].

Summer-type hypersensitivity pneumonitis(SHP) first reported by T. OCHI, et al. (1978), as a new type hypersensitivity pneumonitis(HP) with features of initiation during summer and anti-Cryptococcus antibody positive sera, has been recognized as "a unique disease in Japan", a most common type of HP in Japan, and now also known as anti-Trichosporon cutaneum antibody-positive SHP. This report was mainly concerned with the histopathology of SHP, thus far diagnosed in our hospital. Of the cases in our hospital, 62 consecutive biopsied cases (3 cases of open lung biopsy and 59 cases of transbronchial lung biopsy) without steroid institution before lung biopsy have been reviewed and revealed granulomatous interstitial pneumonitis in the bronchiolo-alveolar region, like various types of HP. Alveolitis (61 of 62 cases; 98.4%), sarcoid-like granuloma (50 of 62; 80.6%) and Masson's body (36 of 62; 58.1%) are main features, and could be named "triad" features. Concerning histopathological findings related with the period of lung biopsy after onset of clinical episodes as HP, alveolitis has been present regardless of period, and fibrinous exudate present in the early period and not in a case at 4 months. Sarcoid-like granuloma and Masson's body have appeared firstly at one-month cases. After this period sarcoid-like granuloma have been present in nearly all cases, but Masson's body has been not present in 10-month case with gradual decrease after 2 months, when all 2-month cases had it. In summary, for histopathological diagnosis of HP, the "triad" features and the time of lung biopsy done are keys, taking into consideration histopathological differential diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alveolitis, Extrinsic Allergic↗
PubMed1981

Delayed type hypersensitivity for penicillin in mice. I. Induction and characterization of delayed type hypersensitivity for penicillin in mice.

The delayed type hypersensitivity (DTH) for benzylpenicilloyl (BPO) group was observed in the footpad swelling reaction (FSR) in mice. Mice were subcutaneously immunized with 300 microgram of BPO-human serum albumin (HSA) conjugate and Freund's complete adjuvant and challenged into footpads with 25 microgram of BPO-bovine gamma globulin (BGG) conjugate 2 weeks after the immunization. The strongest FSR was observed 24 hours after the challenge. This FSR was typical DTH. Namely, the kinetics of FSR and the histological study showed the pattern of the DTH. Furthermore, the FSR could be transferred to normal syngenic mice by transfer of antigen-primed spleen cells and could not be transferred by anti-Thy-1,2-serum treated cells. The DTH for BPO was observed on day 4 after the immunization and reached the maximum on day 11 to 14. Thereafter, the DTH for BPO decreased gradually in proportion as the IgG antibodies for BPO were produced. C57BL/6 and C3H/He mice high responders, A/J mice moderate, and BALB/c and DBA/2 mice were low responders. Penicillins were broad cross-reactive in FSR and its desensitization test because the DTH for penicillins contained the common reactivity for the penicilloyl moiety. The DTH for BPO was suppressed by intravenous preadministration of HSA and this suppression was sensitive to cyclophosphamide.

Animals↗
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↗