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A Bellavia

Publications and source records attributed to A Bellavia.

At least 19 recordsLinked to original sources
PubMed1999

Impaired contact hypersensitivity to trinitrochlorobenzene in interleukin-4-deficient mice.

We have examined the role of endogenously produced interleukin-4 (IL-4) in the contact hypersensitivity (CH) reaction to the haptene trinitrochlorobenzene (TNCB). The CH reaction was abolished in IL-4 genetically deficient mice (IL-4 KO), when compared to wild-type (wt) mice. The CH reaction was restored by treatment with IL-4 and further analysis revealed that IL-4 exerted its action both at the induction and effector stages of the CH reaction. Despite failure to develop a CH reaction, IL-4 KO mice developed a T helper type 1 (Th1) response to TNCB, in terms of lymphokine production in vitro. Furthermore, the number of Vgamma3+ cells accumulating in the lymph nodes of TNCB-immune IL-4 KO mice was normal. The recruitment of mononuclear cells and vascular leakage at the challenge site were consistently reduced in IL-4 KO mice and were restored by injection of IL-4. This suggests that IL-4 acts as a proinflammatory mediator in CH, perhaps favouring the accumulation of mononuclear cells at the site of inflammation. Among Th2-type cytokines, IL-13, but not IL-10, was shown to restore the CH reaction to TNCB in IL-4 KO mice. However, IL-4 KO mice developed a normal CH response to oxazolone, indicating that IL-4 was required for the CH reaction to TNCB, but not for that to oxazolone.

Adjuvants, Immunologic↗
PubMed1997

Three cell subsets are required for the transfer of delayed-type hypersensitivity reaction by antigen-specific T cell lines.

Antigen (trinitrochlorobenzene)-specific T cell lines were obtained by repeated stimulation of lymph node cells from immune mice with antigen in vitro. These T cell lines, consisting of more than 90% CD4+ Vbeta8.2+ and 6 to 9% gammadelta+ T lymphocytes, transfer contact sensitivity (CS) locally when injected at the same site as the challenge antigen, but fail to mediate a systemic passive transfer when injected i.v. Injection of T cell lines together with spleen cells from mice immunized 1 day beforehand (1-day cells) allowed a successful, specific systemic transfer of CS. Phenotypic analysis showed that the 1-day immune cell was alphabeta+, gammadelta-, sIg-, CD3+, CD4-, CD8-, CD5+, B220 (CD45R)+, Thy 1.2+. The effect of 1-day immune cells occurred through a mechanism involving IL-4, as 1-day immune cells failed to allow systemic transfer of CS by T cell lines in recipient mice treated with mAb to IL-4. These observations strongly indicate that three cell subsets are required for the systemic passive transfer of CS by T cell lines: alphabeta+ CD4+, gammadelta+, and a third cell subset, which is CD45R+, alphabeta+, CD3+, but double (CD4, CD8) negative.

Animals↗
PubMed1997

In vivo cimetidine immunomodulatory effects on the cutaneous reaction to oxazolone in the chicken.

The effect of the histamine H2-receptor antagonist, cimetidine, on the cutaneous Arthus-like hypersensitivity to oxazolone elicited injecting subcutaneously oxazolone conjugated to egg-albumin (EA-OX) has been examined in the chicken. Cimetidine had opposite effects on the cutaneous reaction to oxazolone in relation to a different immunization schedule. Cimetidine enhanced the cutaneous reaction to oxazolone obtained immunizing chickens with oxazolone dissolved in ethanol (Eth-OX); instead cimetidine inhibited the cutaneous reaction obtained in chickens immunized with oxazolone dissolved in complete Freund adjuvant (CFA-OX). Optimum enhancement of the cutaneous arthus-like reaction to oxazolone occurred when cimetidine was given for three consecutive days starting at the immunization. The enhancing effect was absent in neonatally bursectomized chickens. Moreover, cimetidine stimulated bursal cell proliferation at day 1 after sensitization. The study of the immunoglobulin class of oxazolone antibodies produced in the immunized chickens demonstrated that cimetidine stimulated the IgM oxazolone antibody synthesis in Eth-OX immunized chickens and inhibited the IgY oxazolone antibody production in Eth-OX and total oxazolone antibody production in CFA-OX immunized chickens. The relationship between increased IgM oxazolone antibody synthesis and enhancement of the cutaneous Arthus reaction is discussed. The role of IgM antibodies in the pathogenesis of Arthus reaction in the chicken is hypothesized.

Adjuvants, Immunologic↗
PubMed1995

Interleukin-4 is a critical cytokine in contact sensitivity.

This study demonstrates an essential role for interleukin-4 (IL-4) in the delayed hypersensitivity reaction, as illustrated by contact sensitivity (CS) to trinitrochlorobenzene (TNCB). Injection of mice with monoclonal antibody to IL-4, but not with control antibody, reduced CS after active immunization by 75%, as judged by ear swelling. The histological alterations of CS were also reduced. IL-4 was essential to the effector stage, as inhibition of its production or action blocked the passive transfer of CS. In particular, treatment of immune lymph node cells with antisense oligonucleotide to IL-4 inhibited the systemic transfer of CS. Transfer was also inhibited by monoclonal antibody to IL-4 given to the recipient. The present results indicate that IL-4 is an essential cytokine at the effector stage of the CS reaction.

Animals↗
PubMed1994

Induction of graft versus host disease in SCID mice by MRL/lpr cell transfer.

We have investigated the graft versus host (GvH) disease induced in immunodeficient SCID (H-2d) mice by intravenous (iv) or intraperitoneal (ip) transfer of either spleen or lymph node cells from autoimmune (MRL/lpr and MRL/++ mice, H-2k) and normal (CBA, H-2k) mice. Rapid and lethal GvH disease was observed when cells from MRL/lpr or MRL/++ were iv transferred into SCID mice, while spleen cells from nonautoimmune CBA donors were partially tolerized into SCID recipients and induced only lower levels of GvH reaction. No GvH reaction (complete tolerance) was observed when CBA lymph node cells were iv transferred into SCID recipients. In contrast, the ip injection of MRL/lpr or CBA spleen cells induces similar levels of GvH. The development of GvH disease in SCID recipients was due to the expansion of alloreactive CD8+ cells displaying significant cytotoxic activity against H-2d, but not against autologous targets. Also, a significant decrease of CD4/CD8 ratio was observed in the course of GvH caused by the iv transfer of cells from MRL/lpr mice. Altogether, these data support the hypothesis that lymphocytes from the MRL/lpr mice may escape tolerance in the GvH reaction.

Animals↗
PubMed1994

Analysis of the adoptive transfer of delayed hypersensitivity and T cell repertoire in severe combined immunodeficiency mice reconstituted with human lymphocytes.

The functional capacity of human T cells to passively transfer delayed hypersensitivity (DH) was analysed in severe combined immunodeficiency (SCID) mice. The tissue distribution of human peripheral blood lymphocytes (PBL) was analysed by 51chromium labelling 1 and 24 h after intravenous cell injection. Labelled PBL from purified protein derivative (PPD)-positive healthy individuals mainly localize in the spleen, liver and lungs, with no arrival in the peripheral lymphoid organs and at the site of antigen challenge (footpad). According to such defective distribution, human PPD-immune cells failed to passively transfer PPD-specific DH to SCID recipients when cells were injected either intravenously or intraperitoneally (systemic transfer). On the contrary, PPD-immune cells were able to transfer DH to PPD when injected directly into the footpad (local transfer). Both memory (CD45RA-) and naive (CD45RA+) enriched subsets were equally able to transfer local DH. The long-term reconstitution of the human immune system in SCID mice was analysed after intraperitoneal PBL transfer (hu-PBL-Scid) by phenotypic analysis, immunoglobulin level, and human DNA detection. Moreover, the reconstitution of the V beta T cell receptor (TCR) repertoire in SCID mice was analysed by anchored polymerase chain reaction (PCR) showing that all the 22 V beta families were expressed in the spleen of hu-PBL-SCID mice. Moreover, scanner analysis of Southern blotting revealed the selective expansion of distinct V beta families (V beta 3, V beta 6, V beta 8, V beta 13.1, V beta 14, V beta 17), suggesting that human lymphocytes could recognize specific antigens or superantigens in the SCID environment.

Animals↗
PubMed1993

Augmented passive transfer of contact sensitivity in severe combined immunodeficiency mice and its dependence of V beta 8+ cells in the picryl system.

The passive transfer of contact sensitivity using picryl chloride immune cells from H-2 syngenic BALB/c donors was analyzed in severe combined immunodeficiency (SCID) mice which lack functional T and B lymphocytes. H-2-restricted and antigen-specific contact sensitivity was transferred to SCID mice, and comparison between the level of contact sensitivity and the number of transferred cells showed a significantly more efficient transfer to SCID than to BALB/c mice. The cells passively transferring contact sensitivity were shown to carry the V beta 8 phenotype. Moreover, chromium-labeled cells from BALB/c PC1-primed donors localize normally in peripheral lymphoid organs and an increased percentage of cell arrival in the ears is clearly observed in SCID after challenge with picryl chloride.

Animals↗
PubMed1992

Contact sensitivity to oxazolone in the chicken: evidence for Arthus type hypersensitivity of the cutaneous reaction.

Cutaneous hypersensitivity reaction can be induced in chickens by skin painting with oxazolone, 33 mg/Kg of body weight (KBW). The B cell contribution to the generation of the cutaneous reaction has been a matter of controversy. In an attempt to characterize this reaction we placed special interest on the possibility that the nature of this reaction could be Arthus type hypersensitivity. From the kinetics study on the cutaneous hypersensitivity after challenge with oxazolonated egg-albumin (EA-OX) it was excluded that the nature of this reaction could be delayed type hypersensitivity. Immune sera transfer experiments demonstrated that the cutaneous reaction was antibody dependent. Serum anti-oxazolone antibody titers in sensitized chickens were assayed by antiglobulin haemagglutination, using oxazolone coupled sheep erythrocytes (OX-SRBC). High titres of IgG were found in contact sensitized chickens. Furthermore this cutaneous reaction was characterized by neutrophils, inflammatory edema, rare thrombotic occlusion of small venules and on absence of monocytes. The utilization of complete Freunds' adjuvant (CFA) given at sensitization demonstrated that CFA enhanced oxazolone antibodies in the sera of immunized chickens without a correlated increase in the intensity of the cutaneous reaction to EA-OX. Animals sensitized to oxazolone (33 mg/KBW) without CFA and challenged intravenously seven days later with oxazolone coupled to autologous chicken red blood cells (OX-CRBC) died from anaphylactic shock; instead animals with the same treatment but with CFA given at sensitization did not die from anaphylactic shock. Taken collectively it was concluded that the cutaneous reaction to oxazolone in the chicken can be categorized as Arthus hypersensitivity. The relationship between cutaneous Arthus reaction and anaphylactic shock in chickens sensitized to oxazolone is discussed.

Anaphylaxis↗
PubMed1987

Effects of dextran sulphate on lymphoblast extravasation into inflammatory skin sites.

The effects of high molecular weight dextran sulphate (DXS) on the migration of 125I-labelled deoxyuridine-labelled peripheral lymphoblasts (stimulated by oxazolone) were studied in vivo by injecting the drug (50 mg/kg) subcutaneously in recipients, and by following the fate of oxazolone-stimulated peripheral lymphocytes treated in vitro with DXS in non-treated syngeneic recipients. Both types of experiments demonstrate that DXS considerably reduces lymphoblast extravasation in skin sites inflamed either by non-immune causes or by DTH. Our results also demonstrate that oxazolone-stimulated peripheral lymphocytes, after in vitro treatment with DXS, are unable to transfer antigen-specific contact hypersensitivity to unsensitized recipients. The results obtained suggest that the drug acts on both T effector cells and lymphoblasts.

Animals↗
PubMed1987

Influence of reserpine on in vivo localization of injected lymph node cells in the mouse.

The effects of reserpine, and other agents that affect the storage and availability of 5-hydroxytryptamine (5HT), on the localization of injected 51Cr-labelled syngeneic lymph node cells have been investigated. A high dose (5 mg/kg) of reserpine to the recipients reduced localization in the lymph nodes and prevented the usual accumulation of lymphocytes in lymph nodes draining the site of an antigen (sheep erythrocytes: SE) injection. These effects were partially reversible by the monoamine oxidase inhibitor nialamide. This dose of reserpine produced deep sedation throughout the period of the experiment. Lower doses, up to 2.5 mg/kg, produced little sedation and had no effect on the localization of lymphocytes. Other workers had previously reported reduced localization of cells in delayed-type hypersensitivity (DTH) lesions after treatment of the recipients with 5 mg/kg reserpine, and had interpreted this in terms of a role of 5HT in promoting vascular permeability and egress of blood cells. The effect of lower doses of reserpine was not reported. We suggest that the effects on cell localization in both sets of experiments may have been secondary to the general state of sedation and not attributable to a direct local influence of 5HT. Other effects of reserpine included prolonged retention of lymphocytes in lungs and blood, and a reduction of cellularity and DNA synthesis in the thymus, spleen and lymph nodes.

Animals↗
PubMed1984

Effects of dextran sulphate (DXS) on lymphocyte localization in complement-deficient mice: evidence that the fifth component of complement is not implicated in the DXS activity.

The effects of subcutaneously or intraperitoneally administered dextran sulphate (DXS) (50 mg/Kg) on the subsequent 1 h localization of intravenously injected radiolabelled lymph node cells was investigated in complement deficient mice which lack C5. DXS proved to be equally as potent in depressing cell localization in deficient as compared to normal mice. These findings indicate that the terminal complement components are not essential for DXS activity.

Animals↗
PubMed1979

Depression of contact hypersensitivity to oxazolone in mice exposed to Newcastle disease virus.

The effect of Newcastle disease virus (NDV) on delayed hypersensitivity to oxazolone in CBA mice was studied. There was a significant impairment of the ability of mice to develop cutaneous hypersensitivity shortly after injection of the virus. The effect was evident when NDV was administered up to 2 days before or within 24 h after sensitization, suggesting that NDV interferes with the process of sensitization. The degree of depression was related to the dose of virus inoculated. NDV inactivated by UV irradiation or heat did not depress contact sensitivity to oxazolone. These data are considered to support the hypothesis that the depression is mediated by a direct interaction between lymphocytes and NDV.

Animals↗
PubMed1977

Delayed-type skin reactions in bursectomized or thymectomized chickens.

Chickens can easily be induced to develop delayed-type skin reactions to oxazolone when animals are sensitized 7 days before the challenge. The reaction is quantitated by assessing the increase in wattle thickness: maximum reactions occur 24 h after challenge. The reaction is inhibited by neonatal thymectomy or bursectomy; these findings therefore suggest also an important B-derived component in delayed hypersensitivity to oxazolone.

Animals↗
PubMed1975

Regulation of antibody formation in chickens escaping from tolerance to human serum albumin.

The immune capacity of chickens made tolerant to human serum albumin just after hatching was studied after a primary and secondary challenge at 7--14 weeks of age, of either 1 mg/kg or 100 mg/kg. The class and avidity of antibody produced by birds "escaping" from tolerance was similar to normal controls. The escaping chickens made a normal peak antibody response to a high dose but not to a low dose (except that the response to a low secondary dose after priming with a high dose was normal); but the decline of the antibody titer was abrupt, indicating inability to maintain the response. It is concluded that the antibody-forming capacity of B cells is normal, but regulation of antibody formation is impaired in previously tolerant chickens.

Animals↗