vicia villosa/hypersensitivity

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Characterization of two different Ly-1+ T cell populations that mediate delayed-type hypersensitivity.

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This paper describes two functionally different T cell populations that mediate delayed-type hypersensitivity (DTH) reactions in contact-sensitized mice. Both of these T cells are Ly-1+, Qa-2-, and Vicia villosa lectin nonadherent. One of these T cell subpopulations is responsible for the classical

HgCl2-induced perturbation of the T cell network in experimental allergic encephalomyelitis. II. In vivo demonstration of the role of T suppressor and contrasuppressor cells.

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In the companion paper (J. Rossert et al., Cell. Immunol. 137, 1991), we showed by using limiting dilution analysis that Lewis (LEW) rats injected with HgCl2 and immunized with myelin (LEWHg/MYE) exhibit anti-basic protein CD4+ T helper cells (Th), at least 10-fold more frequent CD8+ T suppressor

HgCl2-induced perturbation of the T cell network in experimental allergic encephalomyelitis. I. In vitro characterization of T cells involved.

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Mercuric chloride (HgCl2) induces in Lewis (LEW) rats a non-antigen-specific immunosuppression and is able to down-modulate experimental allergic encephalomyelitis in about 70% of the rats. The aim of the present study was to determine the frequencies of lymph node cells involved in the

Cellular interactions in the adoptive transfer of contact sensitivity: characterization of an antigen-nonspecific Vicia villosa-adherent T cell needed for adoptive transfer into naive recipients.

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The adoptive transfer of delayed-type hypersensitivity (DTH) into naive recipients requires the interaction of two functionally distinct Ly-1+ T cells: and I-J- cell effector cell for DTH which transfers antigen-specific DTH only into animals whose suppressive mechanisms have been compromised, and

Hairy vetch (Vicia villosa Roth) poisoning in cattle: update and experimental induction of disease.

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Hairy vetch poisoning (vetch-associated disease) of cattle is a generalized disease characterized pathologically by infiltration of skin and many internal organs by monocytes, lymphocytes, plasma cells, and often eosinophils and multinucleated giant cells and clinically by dermatitis, pruritus,

Oral tolerance to dextrin mediated by specific suppressor T-cells induced in the intestinal intraepithelium and their systemic migration.

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Antigens presented to the immune system through the oral route induce antigen specific secretory IgA and systemic unresponsiveness, termed oral tolerance (OT). We studied the induction of OT towards a diet antigen: dextrin (DEX) in rats that underwent protein deprivation and were further re-fed.

Down-regulation of suppressor cell induction.

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A unidirectional cascade of cell interactions has been described previously that involves at least three distinct populations of suppressor T cells (Ts) that interact in appropriate succession to mediate suppression of delayed hypersensitivity responses to the 4-hydroxy-3-nitrophenylacetyl hapten

Characterization of an immunoregulatory cell subset involved in the up-regulation of the autoimmune response to rat male accessory glands.

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OBJECTIVE We studied the regulation of the autoimmune response to rat male accessory glands (RAG) using liposomes as adjuvants. METHODS Adult male Wistar rats were submitted to three intraperitoneal (i.p.) immunizations with 750 micrograms of saline extract of RAG associated with liposomes. The

Immunoregulatory circuits which modulate responsiveness to suppressor cell signals: contrasuppressor cells can convert an in vivo tolerogenic signal into an immunogenic one.

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The intravenous injection of 2,4,6-trinitrophenyl (TNP)-labeled peritoneal exudate cells (TNP-PEC) into CBA mice fails to produce a state of hypersensitivity; rather, it renders recipient mice incapable of mounting a contact hypersensitivity response when they are subsequently immunized with a

Immunoregulatory role of Ig isotypes. II. Activation of cells that block induction of contact sensitivity responses by antibodies of IgG2a and IgG2b isotypes.

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The influence that the isotype of Ag-specific antibody has on the induction of contact hypersensitivity (CS) has been investigated. Injection (i.v.) of mice with haptenated peritoneal exudate cells (PEC) pretreated with anti-hapten mAb of the IgG2a and IgG2b isotypes results in the activation of

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