Disease relevance of Trinitrochlorobenzene

• We examined the role of cytokines in the cutaneous response to the application of trinitrochlorobenzene (TNCB) in both nonsensitized and sensitized mice, i.e., in the irritant reaction (IR) and contact hypersensitivity reactions (CH) [1].
• 26.10.2 TsF suppresses the passive transfer of delayed-type hypersensitivity (DTH) mediated by DNP- but not trinitrochlorobenzene- or oxazalone-primed DTH T cells (TDH) after a 1 hr incubation at 37 degrees C. In contrast, 26.10.2 TsF had no suppressive effect on secondary in vitro DNP-specific T cell proliferative responses [2].
• The scratching counts were significantly increased only 1 week after housing the mice under conventional conditions, but no changes were observed in cases of TNCB-induced dermatitis [3].
• 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) [4].
• Early pregnancy factor treatment suppresses the inflammatory response and adhesion molecule expression in the spinal cord of SJL/J mice with experimental autoimmune encephalomyelitis and the delayed-type hypersensitivity reaction to trinitrochlorobenzene in normal BALB/c mice [5].

High impact information on Trinitrochlorobenzene

• In contrast, IL-1beta-deficient mice showed defective contact hypersensitivity responses to topically applied trinitrochlorobenzene (TNCB) [6].
• To show that anergy induction by IL-10 was antigen-specific, mice initially treated with IL-10 plus TNCB were exposed to 0.5% dinitrofluorobenzene (DNFB) 14 d later (group 1) [7].
• We demonstrate that the cells that transfer CHS to TNCB adhere to FN in the presence of Ca2+/Mg2+, and T-cell populations depleted of FN-adherent cells do not transfer immunity [8].
• We have examined directly the role of T-cell integrins in vivo by using the well-characterized, T-cell-mediated contact hypersensitivity (CHS) response to the hapten trinitrochlorobenzene (TNCB) [8].
• To delineate the mode of action of such vaccines, we used trinitrophenyl, the antigenic moiety of the contact allergen trinitrochlorobenzene, as surrogate Ag [9].

Chemical compound and disease context of Trinitrochlorobenzene

• Analysis of dose response of trinitrochlorobenzene contact hypersensitivity induction in mice: pretreatment with cyclophosphamide reveals an optimal sensitizing dose [10].
• To determine whether macrophage migration inhibitory factor (MIF) is required for contact hypersensitivity (CHS) response, MIF-deficient (MIF KO) and wild-type (WT) mice were sensitized with trinitrochlorobenzene (TNCB) or oxazolone on their abdominal skin and challenged on the dorsum skin of one ear 5 days later [11].
• Most importantly, however, we demonstrate that TNP attached to lysine 97 in the staphylococcal nuclease peptide 93-105 (i.e. a clearly "non-self" sequence) is able to prime mice for subsequent elicitation of contact sensitivity by TNCB in the absence of foreign protein [12].
• Application of the contact sensitizer, DNFB, through skin depleted of LC (by pretreatment with either the carcinogen DMBA or the antigen TNCB) failed to induce contact sensitivity [13].
• OBJECTIVE: To investigate whether the Th1-dominant response has an influence on the development of AD, we induced chronic allergic hypersensitivity with 2,4,6-trinitrochlorobenzene (TNCB ) in two AD mouse models: NC/Nga mice and DS-Nh mice [14].

Biological context of Trinitrochlorobenzene

• CHS to TNCB, detected as an increase in ear thickness 24 h after epicutaneous challenge, was significantly enhanced in major histocompatibility complex class II-deficient mice compared with wild-type controls [15].
• We undertook a detailed analysis of the dose-response and kinetics of UV-induced local and systemic suppression of contact hypersensitivity to trinitrochlorobenzene in two strains of mice, C57BL/6 and BALB/c. We found that the UV dose-responses for systemic and local suppression were identical within the same strain [16].
• Early down-regulation of host granulomatous response to subcutaneously implanted cotton string and delayed-type hypersensitivity (DTH) response to trinitrochlorobenzene (TNCB) was followed later during infection by normalization of these parameters compared to that seen in uninfected mice [17].
• Expression of the murine glyceraldehydephosphate dehydrogenase (GAPDH) gene, a candidate internal control, was not constant in cells from trinitrochlorobenzene- and vehicle-applied animals, suggesting that GAPDH gene expression changes in heterogeneous lymph node-cell subsets during induction of contact hypersensitivity [18].
• Suppressive effect of acupuncture on delayed type hypersensitivity to trinitrochlorobenzene and involvement of opiate receptors [19].

Anatomical context of Trinitrochlorobenzene

• Four days after painting mice with 7% trinitrochlorobenzene, draining lymph node cells were obtained and T cells were purified [20].
• Suppression induced by feeding TNCB is hapten specific and can be transferred to normal animals with lymphoid cells from fed mice [21].
• We recently described a method for inducing immunologic tolerance to trinitrochlorobenzene (TNCB), a hapten that generates suppressor cells capable of down-regulating the efferent phase of TNP-specific contact hypersensitivity in rats [22].
• Mice whose skin was painted with trinitrochlorobenzene (TNCB) exhibited a variety of anti-TNP T cell responses, including delayed-type hypersensitivity (DTH) and cytotoxic T cell responses, as well as helper T cell activity [23].
• The hybridomas were used to detect hapten-bearing APC in draining lymph nodes of mice sensitized with trinitrochlorobenzene or FITC in vivo [24].

Associations of Trinitrochlorobenzene with other chemical compounds

• To investigate whether IL-10 also subserves the function of a tolerizing agent in vivo ears of BALB/c or C3H mice were injected intradermally with 1-2 micrograms of recombinant mouse (rm)IL-10 8 h before epicutaneous application of 3% trinitrochlorobenzene (TNCB; a contact allergen) [7].
• C3H/He mice were allowed to generate the amplified (more potent) TNP-helper T cell activity by skin painting with trinitrochlorobenzene (TNCB) after pretreatment with cyclophosphamide [25].
• UVA irradiation suppressed the endogenous proliferation of lymph node cells in trinitrochlorobenzene-painted mice, and this suppression was significantly reversed by the application of glutathione to the skin during irradiation [26].
• A murine epidermal cell suspension was exposed to UVA in vitro, pulsed with trinitrobenzenesulfonic acid, and cultured with T cells prepared from syngeneic mice previously sensitized with trinitrochlorobenzene [26].
• Analysis of the kinetics of MMP-9 expression showed that its production was induced within 6 hr after application of 2,4,6-trinitrochlorobenzene (TNCB), substantially increased between 12 hr and 24 hr, and then decreased to the normal level by 7 to 10 days [27].

Gene context of Trinitrochlorobenzene

• Repetitive topical application (weekly for six consecutive weeks) of trinitrochlorobenzene to their ears also elicited a stronger cutaneous inflammation in keratin 5/interleukin 18 transgenic mice than seen in immunoglobulin/interleukin 18 transgenic or wild-type mice [28].
• Impaired contact hypersensitivity to trinitrochlorobenzene in interleukin-4-deficient mice [29].
• It is concluded that oxazolone- and TNCB-induced contact hypersensitivity is partially dependent on a functional IFN gamma system [30].
• Only B7-1 transgenic mice exhibited significant immediate type ear swelling responses to the hapten trinitrochlorobenzene [31].
• In contrast to the immediate-type response, the delayed-type hypersensitive response, observed as a thickening of the ear skin after trinitrochlorobenzene challenge (following sensitization), showed no differences between HDC+/+ and HDC-/- mice [32].

Analytical, diagnostic and therapeutic context of Trinitrochlorobenzene

• Feeding TNCB induces an efferent-acting suppressor T cell (Ts eff), as well as an intermediary acceptor T cell (T acc) with which it interacts to block adoptive transfer of CS with immune cells [21].
• At 24 h after application of 3% trinitrochlorobenzene, LC appear larger and exhibit more intense staining in epidermal sheets using anti-I-A antibodies, and there was a two- to threefold increase in I-A and I-E expression by LC using flow microfluorimetry analysis [33].
• To identify the EC sources of immunosuppression in this system, we examined the effect of UVB on the capacity of EC to induce and to regulate CH to trinitrochlorobenzene (TNCB) [34].
• Small-animal PET and autoradiography with the alpha(v)beta(3) ligands (18)F-galacto-RGD and (125)I-gluco-RGD were performed at various times after TNCB application [35].
• The subcutaneous injection of major histocompatibility complex class II-specific, but not of class I-binding, hapten-derivatized peptides in incomplete Freund's adjuvant induced specific, albeit low, contact hypersensitivity responsiveness to trinitrochlorobenzene [36].

References