Disease relevance of picric acid

• In vitro and in vivo studies of a 2,4,6-trinitrophenyl (TNP)-binding immunoglobulin A (IgA) lymphoma isolated from MOPC-315, a TNP-binding IgA plasmacytoma of BALB/c mice [1].
• The results show that adult thymectomy prevents the inhibition of trinitrophenol (TNP)-specific delayed-type hypersensitivity, which normally occurs after injection of TNP-BSA into the anterior chamber (AC) of the eye [2].
• A severe, Th1-mediated experimental colitis with similarities to inflammatory bowel disease in humans can be induced by a single injection of 2,4,6-trinitrophenol (TNP)-substituted protein plus adjuvant in IL-2-/- mice [3].
• MOPC 315 is a BALB/c plasmacytoma which secretes a trinitrophenol-binding IgA lambda 2 paraprotein [4].
• Animals that rejected TNP-1591-RE and subsequently TNP-3152-PRO tumor cells showed increased tumor-specific resistance to another challenge of 3152-PRO tumor cells, even when these fibrosarcoma cells had not been haptenated with TNP [5].

Psychiatry related information on picric acid

• The responses to 2,4,6-trinitrophenyl conjugates of different Ficoll preparations differ with respect to the magnitude of the accompanying auto-anti-idiotype (Id) response in both mice and chickens [6].

High impact information on picric acid

• We analysed the diversity of TCRs in a collection of H-2Kb-restricted, 2,4,6-trinitrophenyl (TNP)-specific (H-2Kb/TNP) cytotoxic T-cell (Tc) clones from C57BL/6 mice [7].
• In these experiments, self-MHC-restricted CTLs differentiate form spleen cells of nu/nu mice which lack thymuses after stimulation with 2,4,6-trinitrophenyl (TNP)-coupled autologous cells in the presence of T-cell growth factor [8].
• The resulting cells lysed 2,4,6-trinitrophenyl chicken erythrocytes (TNP CRBC) in a hapten-specific manner [9].
• BALB/cB cells specific for 2,4,6-trinitrophenyl (TNP) were isolated from spleens of immune mice by elution from TNP-gelatin-coated dishes [10].
• Definition of conditions that enable antigen-specific activation of the majority of isolated trinitrophenol-binding B cells [11].

Chemical compound and disease context of picric acid

• Rhodococcus erythropolis HL 24-2, which was originally isolated as a 2,4-dinitrophenol-degrading bacterium, could also utilize picric acid as a nitrogen source after spontaneous mutation [12].
• A strain of Pseudomonas aeruginosa reduced 2,4,6-trinitrophenol (picric acid) to 2-amino-4,6-dinitrophenol (picramic acid) under anaerobic conditions [13].
• In previous studies, we have shown that the oral administration of colonic proteins that have been haptenated (i.e., haptenated colonic proteins [HCPs]) with trinitrophenol (TNP) can protect mice from the subsequent induction of trinitrobenzene sulfonic acid colitis [14].
• The studies show that in vitro stimulation of naive A/J spleen cells with the thymic-independent antigen, Brucella abortus, to which TMA and trinitrophenol (TNP) or fluorescein (FL) are coupled (TMA-BA-TNP or TMA-BA-FL), induces significant numbers of anti-TNP or anti-FL plaque-forming cell (PFC) responses [15].
• The immunostaining patterns were compared with the appearances seen in adjacent sections stained by the routine haematoxylin and eosin (H & E) and phosphotungstic acid haematoxylin (PTAH) methods and a method previously recommended for the detection of early myocardial infarction, the haematoxylin basic fuchsin picric acid (HBFP) stain [16].

Biological context of picric acid

• Colchicine (CC) enhances the antibody response in mice to protein antigens, like diphtheria toxoid and human gamma globulin, as well as to the 2,4,6-trinitrophenyl hapten [17].
• Cells stimulated with picric acid in the presence of high extracellular Mg2+ showed very few sites of membrane fusion and no tmx expansion, suggesting that Ca2+ is required for both membrane fusion and tmx expansion [18].
• We have previously shown that down-regulation by Ts cells after AC injection with 2,4,6-trinitrophenol (TNP)-coupled spleen cells (TNP-Spl) is initiated by the intraocular activation of Ts inducer cells [19].
• Up to now, only initial ring hydrogenation of picric acid (2,4,6-trinitrophenol) opens perspectives of complete degradation [20].
• Solution studies indicate tighter binding of picric acid in the active sites of the W102Y and W102F enzymes [21].

Anatomical context of picric acid

• To address this issue, 42 H-2Kb-restricted, 2,4,6-trinitrophenyl (TNP)-specific cytotoxic T-cell (Tc) clones from C57BL/6 mice were characterized with respect to expression of different beta-chain gene segments in messenger RNA using specific oligonucleotide probes [22].
• This study establishes that dendritic cells (DC) are the critical accessory cells for the development of anti-trinitrophenol (TNP) cytotoxic T lymphocytes (CTL) in vitro [23].
• Primed T cells were then tested for helper activity in the in vitro response of B cells and macrophages (Mphi) of parental or F1 origin to the hapten trinitrophenol coupled to the priming antigen [24].
• To this end, we selected two hybridomas, called Id(3) and Id(A.01), that produce immunogenic IgM(lambda)2 directed toward 2,4,6-trinitrophenyl, and subcloned rare IgG1, IgG3, IgE, or IgA class switch variants [25].
• Phosphatidylethanolamine bearing the 2,4,6-trinitrophenyl hapten was introduced into the surface membrane of mammalian fibroblasts by incubating the cells with small unilamellar vesicles containing this hapten-conjugated lipid [26].

Associations of picric acid with other chemical compounds

• Simultaneous injection of 2 X 10(7) gamma-irradiated or glutaraldehyde-fixed RCS cells with the antigen sheep red blood cells (SRBC) or 2,4,6-trinitrophenol (TNP)-Ficoll markedly suppressed the subsequent plaque-forming cell response in the spleen [27].
• This high-resolution analysis indicates that the active site is partially occupied with picric acid and that the anomalous density seen in the original study is attributed to the population of multiple conformational states of Trp-102 and not a formal covalent bond between the indole ring of Trp-102 and picric acid [21].
• The kinetics of responses to bacterial lipopolysaccharide (LPS) in both B cell subpopulations were determined in three assay procedures: 1) incorporation of radioactive thymidine into DNA; 2) incorporation of radioactive leucine into immunoglobulin; 3) enumeration of cells forming polyclonal antibody to the 2,4,6-trinitrophenyl hapten [28].
• The low-melting polymorphic modification of the 1:1 complex of benzocaine (BC) and picric acid (PA) had earlier been reported to be an example of a "disappearing polymorph". The BC:PA system has been reinvestigated by thermomicroscopy, calorimetry, solid-state NMR, and X-ray crystallography [29].
• A similar result was obtained when a monoclonal antibody directed against a single plasma membrane glycoprotein was used, or when the rate of surface loss of TNP groups unoccupied by antibodies was measured [30].

Gene context of picric acid

• In contrast, CD40-/- mutant mice responded normally to the T cell-independent (TI) antigens, 2,4,6-trinitrophenyl (TNP)-LPS and TNP-Ficoll [31].
• In vivo, intracameral injection of normal or TNFR1(-/-) 2,4,6-trinitrophenyl-coupled T cells into normal mice induced immune deviation, but TNFR2(-/-) 2,4,6-trinitrophenyl-coupled T cells were ineffective [32].
• When IL-4-deficient mice and normal littermates were immunized with 2,4,6-trinitrophenyl (TNP)-specific IgE followed by bovine serum albumin (BSA)-TNP or with BSA-TNP alone, the BSA-specific IgG1 and IgG2a responses were equally well augmented by IgE in all mice [33].
• Gene-targeted mice lacking the IL-2 gene (IL-2 -/- mice) develop various forms of autoimmunity as well as severe colitis, either spontaneously in a conventional environment or after immunization with 2,4,6-trinitrophenol (TNP)-conjugated keyhole limpet hemocyanin (KLH) in a specific pathogen-free environment [34].
• Hybridoma collections from IL5-activated splenic B cells and LPS-activated B cells were screened and compared for the production of autoantibodies and antibodies directed against the haptens (4-hydroxy-3-iodo-5-nitrophenyl)acetyl (NIP) and 2,4,6-trinitrophenyl (TNP) [35].

Analytical, diagnostic and therapeutic context of picric acid

• Recently, we have examined the mechanisms by which intravenous injection of trinitrophenol-coupled spleen cells leads to systemic tolerance [36].
• The picric acid assay overestimated serum creatinine, when directly compared with the HPLC assay [37].
• To determine the tolerance (or immunity), antibody concentrations in the supernatant fluids were measured by using a TNP-specific ELISA assay [38].
• The antibody production of both 2,4,6-trinitrophenyl-keyhole limpet haemocyanin-primed splenocytes and B cell hybridomas was markedly reduced; about 20-40% of splenocytes and B cell hybridomas were killed by co-culture with IL-6-treated Mm1 [39].
• The primary response was studied after subcutaneous injection of 1 mg of particle together with 10 microgram of reporter antigen TNP-OVA (2,4,6-trinitrophenyl coupled to ovalbumin) into the hind paw [40].

References