Disease relevance of Picryl chloride

• The I-J subregion codes for determinats on suppressor factor(s) which limit the contact sensitivity response to picryl chloride [1].
• T cells able to mediate specific delayed type hypersensitivity (DH) in mice in response to the haptens azobenzenearsonate (ABA), oxazolone (OX), and picryl chloride have been grown in continuous cultures [2].
• Mice lose demonstrable delayed hypersensitivity (DH) to DNFB, picryl chloride, or sheep red blood cells [3].
• The groups tested early during immunotherapy with BCG and allogeneic leukemic blasts were hyper-responsive (compared to published data) to primary sensitization with picryl chloride [4].
• Pulmonary fibrosis was induced by priming hamsters for contact hypersensitivity responses with an epicutaneous application of 2,4,6-trinitro-1-chlorobenzene (TNCB) in carrier and challenging intratracheally (IT) 5 days later with a single dose of the soluble form of the immunizing hapten [5].

High impact information on Picryl chloride

• The titers, measured by passive cutaneous anaphylaxis in rats, increased after repeated applications of picryl chloride [6].
• In contrast, oral administration of trinitrobenzene sulfonic acid (TNBS) to Peyer's patch-null mice resulted in reduced TNBS-specific serum Abs and splenic B cell antitrinitrophenyl Ab-forming cell responses after skin painting with picryl chloride [7].
• The effect of interferon on delayed-type by persensitivity to picryl chloride and sheep erythrocytes was examined in the mouse [8].
• This paper describes the development of Ag-specific proliferation and the production of IFN-gamma and IL-2 during contact sensitivity (CS) to the hapten picryl chloride (PCl) [9].
• These peptides, which we had previously shown to induce contact sensitivity to picryl chloride in vivo regardless of sequence homologies to mouse proteins, were found to activate carrier-independent TNP-specific T cells in vitro [10].

Chemical compound and disease context of Picryl chloride

• Cyclophosphamide treatment (150 mg/kg) of BALB/c mice 48 h before sensitization with picryl chloride (PCl) resulted in striking blood and tissue eosinophilia, maximal at 13 days [11].
• The s.c. injection of 10 mM 2,4,6-trinitrobenzene sulfonic acid (TNBS) derivatized splenic adherent cells (SACs) into syngeneic mice primes for contact sensitivity or delayed-type hypersensitivity (DTH) when these animals are challenged with picryl chloride on the ear or trinitrophenol (TNP)-coupled cells in the footpad, respectively [12].
• Contact sensitivity (CS) to 2,4-dinitrofluorobenzene (DNFB) and picryl chloride (PCl) and contact photosensitivity (CPS) to tetrachlorosalicylanilide (TCSA) were significantly augmented when challenged or sensitized at sites treated with acetone 24 h before, compared with the intact skin [13].
• Oral administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS), a water-soluble analog of trinitrochlorobenzene (TNCB), causes suppression of contact sensitivity (CS) to picryl chloride [14].
• IA+ and IE+ keratinocytes were detected, using an indirect immunofluorescence assay on epidermal sheets, only after the induction and elicitation of contact sensitivity with the sensitizers oxazalone, picryl chloride and 2,4-dinitrochlorobenzene but not with formaldehyde [15].

Biological context of Picryl chloride

• Treatment by the transfection of STAT6 decoy oligodeoxynucleotides (ODN), after the induction of 2,4,6-trinitrochlorobenzene or other haptens had a significant inhibitory effect on the induction of both acute CHS and chronic CHS [16].
• The reverse was found after pretreatment of mice with TNP-labeled isologous IgG (MGG) since only anti-TNP antibody responses, but not contact sensitivity to picryl chloride, were significantly reduced [17].
• XPC mice, which were defective in global genome repair, were as sensitive to ultraviolet-B-induced local suppression of contact hypersensitivity to picryl chloride as their wild-type littermates [18].
• During pregnancy in mice, cell-mediated immunity as measured by a contact allergic reaction to picryl chloride was diminished (P less than 0.001) [19].
• The ability to produce antigen-specific down-regulation of an established immune response was investigated in 2,4,6-trinitrochlorobenzene (TNCB)-immune mice by delivery of antigen through chemical carcinogen- or ultraviolet B (UVB)-treated skin [20].

Anatomical context of Picryl chloride

• In addition, this restriction was also demostrated in CBA (H-2 K) mice and for tolerance in the 1-chloro-2,4,6-trinitrobenzene contact sensitivity system using trinitrophenyl-modified lymphoid cells [21].
• The biphasic patterns of DTH to both tumor cells and picryl chloride and the T cell and mast cell dependence of both antitumor resistance and DTH to tumor cells suggest that T cell-dependent activation of mast cells to allow entry of mononuclear leukocytes into sites of tumor growth is similar to the mechanism that occurs in DTH [22].
• Lymph node cells of CBA (H-2k), but not of BALB/c (H-2d) mice immunized epicutaneously with picryl chloride secrete interleukin (IL)-5 when stimulated with the specific antigen in vitro [23].
• We examined epidermal Langerhans cells at the site of contact with picryl chloride or oxazolone in BALB/c and C57B1/6 mice with regard to their responding to either subsensitizing or sensitizing doses of allergen [24].
• Challenge with 1 % PCl, but not croton oil caused preferential eosinophil accumulation into the dermis, which was associated with the enhanced expression of vascular cell adhesion molecule 1 (VCAM-1) on endothelial cells [11].

Associations of Picryl chloride with other chemical compounds

• 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 [25].
• PC1-F initiates PC1 CS by mediating an early 2-h skin swelling reaction that is due to local release of the vasoactive amine serotonin (5-HT) by mast cells, and perhaps other 5-HT-containing cells [26].
• The DNFB and PCl application in sensitizing doses to nonsensitized animals resulted in a cellular activation similar to that observed for 0.5% croton oil [27].
• TNP-specific TABM in the sera of mice receiving an intracameral injection of TNP spleen cells, followed by contact sensitization with picrylchloride (PCl), were purified by affinity for TNP and were resolved by polyacrylamide gel electrophoresis and immunoblotting as M(r) 110,000 polypeptides [28].
• Mice pretreated with cyclophosphamide have an increased ability to produce anti-trinitrophenyl cytotoxic T cells after painting with the contact sensitizing agent picryl chloride [29].

Gene context of Picryl chloride

• Activation of Lyt-2+ picryl chloride (PC1)-specific cloned T cell lines by trinitrophenyl (TNP)-coupled spleen cells results in proliferation and the production of at least two lymphokines: lymphotoxin (LT) and IFN-gamma [30].
• The PCl-6 T cell line, derived from mice sensitized by skin painting with picryl chloride (PCl), shows antigen dependence for DNA synthesis and for lymphotoxin (LT) production [31].
• In this report, to elucidate roles of IL-1alpha and IL-1beta in CHS, we analyzed ear swelling in 2,4,6-trinitrochlorobenzene (TNCB)-induced CHS using gene-targeted mice [32].
• Using cDNA microarray technology, the expression of chemokine genes in the elicitation site of 2,4,6-trinitrochlorobenzene-induced contact hypersensitivity (CHS) was examined in mice [33].
• The low IL-5 production in BALB/c mice persists when either picryl chloride or the unrelated antigen oxazolone are used, when the amount of antigen in vitro is varied and when a secondary response is studied [23].

Analytical, diagnostic and therapeutic context of Picryl chloride

• The effect of adult thymectomy on antibody production and on the development of contact sensitivity to picryl chloride in mice of different ages was studied [34].
• Mice were sensitized on the lower back skin with picryl chloride between 0 and 25 d, after anagen induction by depilation, and challenged on the earlobes with picryl chloride 5 d later [35].
• To determine if levels of LC E-cadherin are modulated during LC emigration from epidermis, we utilized flow cytometry to evaluate E-cadherin expression on BALB/c LC exposed in situ to the contact allergen 2,4,6-trinitrochlorobenzene (TNCB) [36].
• Results Passive immunization with TNP-specific IgLC resulted in an increase in ear swelling 2 h after PCl challenge [37].
• Contact hypersensitivity to the low molecular weight compound picrylchloride was used as a model for cellular immunity that can be suppressed by low (i.e. suberythemal) doses of UV light even after exposure at a distant locus (i.e. systemic immunosuppression) [38].

References