nitrophenols has been researched along with Dermatitis--Contact* in 7 studies
7 other study(ies) available for nitrophenols and Dermatitis--Contact
Article | Year |
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Equivalence of conventional anti-picryl T suppressor factor in the contact sensitivity system and monoclonal anti-NP TsF3: their final non-specific effect via the T acceptor cell.
There is considerable confusion over whether the antigen-specific T suppressor factors (TsF) described by different authors are indeed equivalent. This paper investigates whether monoclonal TsF3, obtained from hybridomas derived from mice injected subcutaneously with NP derived spleen cells, is functionally equivalent to the conventional T suppressor factor, produced by mice injected intravenously with chemically reactive, water soluble haptene (picrylsulphonic acid and oxazolone thioglycolic acid). Comparison of monoclonal anti-NP TsF3 with conventional anti-picryl and anti-oxazolone T suppressor factor showed that both armed the non-specific T acceptor cell (Tacc) which was sensitive to cyclophosphamide and adult thymectomy. Moreover, non-specific inhibitor (nsINH) of the transfer of contact sensitivity was released when antigen, together with major histocompatibility complex products (MHC), reacted with conventional or monoclonal TsF on the surface of the non-specific T acceptor cell. The interaction of monoclonal TsF3 with antigen, which led to the release of NsINH, required the presence of MHC and was I-J restricted. However, there was no Igh-1 restriction. The equivalence of conventional anti-picryl and anti-oxazolone TsF has been demonstrated by arming the Tacc with a mixture of these two suppressor factors, and then triggering the release of nsINH with the mixed haptene 'picryl-oxazolone-lysine' which crosslinks separate molecules of TsF. A similar equivalence of conventional anti-oxazolone TsF and monoclonal anti-NP TsF3 was demonstrated using the mixed hapten 'NP-oxazolone-lysine' to trigger the release of nsINH. It was concluded that monoclonal TsF3 and conventional TsF were equivalent, and that both had an indirect mode of action through the non-specific T acceptor cell which led to the production of non-specific inhibitor. Topics: Animals; Cyclophosphamide; Dermatitis, Contact; Haptens; Hybridomas; Immunization, Passive; Lymphokines; Major Histocompatibility Complex; Mice; Mice, Inbred Strains; Nitrophenols; Oxazolone; Phenylacetates; Picryl Chloride; Suppressor Factors, Immunologic; T-Lymphocytes; Thymectomy | 1984 |
Fine-specificity of the contact sensitivity to 4-hydroxy-3-nitrophenyl acetyl (NP).
Dorf and colleagues (1-4) found that the contact sensitivity (CS) primed with (4-hydroxy-3-nitrophenyl)acetyl (NP) could be elicited as easily with the iodoanalog (NIP) as with NP when studied in Igh-1b mice but could only be elicited with NP, not NIP, in Igh-1j mice. Since this fine-specificity was parallel to the fine-specificity of anti-NP antibodies in the two types of mice and since anti-NP antibodies of Igh-1b mice are controlled by gene Igh-NPb the authors concluded that CS also was controlled by the Igh-NPb gene. The aim of this study was to confirm their findings with a more quantitative method (5). We confirmed equality of NP and NIP as elicitors of NP-primed CS in Igh-1b mice when the priming antigen was given subcutaneously into non-cyclophosphamide-treated mice (their method). We also found that this priming induced an anti-NP antibody response detectable at the time of challenge. Most experiments were carried out with a method that does not induce a detectable antibody response (pretreatment of mice with 200 mg/kg of cyclophosphamide; application of the sensitizing compound on skin). Since the NP-primed (and NBrP-primed) CS reactions exhibited "expected specificities," the immunizing compound was clearly the most efficient elicitor (relative efficiencies of homologs varied from 2 to 4). The Igh-NPb gene appears not to have a role in "antibody-free" reactions. Topics: Animals; Cross Reactions; Cyclophosphamide; Dermatitis, Contact; Epitopes; Hypersensitivity, Delayed; Immunity, Cellular; Mice; Nitrophenols; Phenylacetates | 1983 |
Hapten-pullulan conjugate-induced CMI suppression: demonstration of a common pathway of suppressor cells involving idiotypic interactions.
Topics: Animals; Dermatitis, Contact; Dinitrobenzenes; Epitopes; Glucans; Immune Tolerance; Immunity, Cellular; Immunoglobulin Idiotypes; Kinetics; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Nitrophenols; Phenylacetates; Receptors, Immunologic; T-Lymphocytes, Regulatory | 1982 |
H-2K-, H-21- and H-2D-restricted hybridoma contact sensitivity effector cells.
Topics: Animals; Antigens, Surface; Cross Reactions; Dermatitis, Contact; H-2 Antigens; Haptens; Hybridomas; Immunity, Cellular; Major Histocompatibility Complex; Mice; Nitrophenols; Succinimides; T-Lymphocytes | 1982 |
[Analysis of immunological tolerance to TNCB contact sensitivity and anti-TNP antibody response (author's transl)].
Topics: Animals; Antibody Formation; Chlorobenzenes; Dermatitis, Contact; Female; Immune Tolerance; In Vitro Techniques; Mice; Nitrobenzenes; Nitrophenols; Trinitrobenzenes | 1978 |
DNA synthesis in vitro during contact sensitivity in the mouse.
Topics: Animals; Carbon Radioisotopes; Dermatitis, Contact; DNA; Drug Hypersensitivity; Epitopes; Lymph Nodes; Lymphocyte Activation; Male; Mice; Mice, Inbred CBA; Nitrophenols; Picryl Chloride; Serum Albumin, Bovine; Skin; Thymidine; Time Factors; Tritium | 1973 |
Evidence for a preferential effect of cyclophosphamide on B-cells.
Topics: Animals; Antibody Formation; Antigens; Antilymphocyte Serum; B-Lymphocytes; Cyclophosphamide; Dermatitis, Contact; Guinea Pigs; Hypersensitivity, Delayed; Immunity, Cellular; Lymph Nodes; Mice; Mitosis; Nitrophenols; Ovalbumin; Skin Tests; Spleen; Splenectomy; T-Lymphocytes; Tuberculin Test | 1973 |