Disease relevance of Ts3

• The genetic restrictions of the activation of third-order suppressor cells (Ts3) were studied in mice, using two different types of anti-azobenzenearsonate (ABA)-immune responses, namely delayed-type hypersensitivity (DTH) and cytotoxic T lymphocyte (CTL) generation [1].
• Therefore, macrophages derived from Early or Late schistosome granulomas or normal spleens are apparently phenotypically indistinguishable and equally capable, in extremely small quantities, of inducing NP-specific DTH, Ts1, and Ts3 immune responses [2].
• We evaluated the ability of these hybridomas to induce third order or effector Ts (Ts3) to suppress the contact sensitivity response against the hapten 4-hydroxy-3-nitrophenyl acetyl (NP) [3].

High impact information on Ts3

• The Ts3 subset of suppressor cells is generated after antigen priming, but, in order to express suppressor activity these cells require an additional activation step involving triggering with specific suppressor factors (TsF2) [4].
• This report characterizes two cloned hybridoma cell lines (pTs3 hybridomas) that represent this stage of Ts3 cell differentiation [4].
• First, heterogeneous populations of F1 Ts3 cells were activated in vitro and then assayed in Ts3-depleted recipients which carried different combinations of H-2 and Igh alleles [5].
• We have found that an I-J+ I-A- antigen-presenting cell (APC) is required for Ts3 activation in vivo [6].
• This selective activation of Ts3 suggested the existence of I-J-related antigen presentation for suppression as the counterpart of I-A or I-A-I-E-restricted antigen presentation for positive immune responses [1].

Chemical compound and disease context of Ts3

• In contrast to the parental P388D1 and two other macrophage hybridomas, one macrophage hybridoma clone, termed 63, when conjugated with NP, induced Ts3, which suppressed contact sensitivity responses against NP but not DNFB, showing that the Ts3 were antigen specific [3].
• The suppressive potential was then tested in mice previously primed for delayed-type hypersensitivity responses which were also treated with cyclophosphamide to deplete Ts3 and other drug-sensitive Ts cell types [7].

Biological context of Ts3

• Since the mode of induction and the phenotype of the third C. neoformans-specific suppressor cells are similar to those reported for Ts3 cells in other antigen-specific suppression models, we referred to this third suppressor cell in the C. neoformans-specific suppressor cell cascade as a Ts3 cell [8].
• Although H-2-linked Ir genes control the development of helper T cells and hapten-specific B cells, they do not influence Ts3 generation [9].
• As suggested by our previous studies on lymphokine production, the results obtained were consistent with direct impairment of Th-cell function and/or with tumour-induced suppression of cell-mediated immunity by Cy-insensitive suppressor cells, such as the 'Ts effector' (Ts3) or those of non-T-cell lineage [10].

Anatomical context of Ts3

• The involvement of a third-order suppressor T cell population (Ts3) in the suppression of in vitro PFC responses was analyzed [11].
• These results are discussed with respect to T cell-mediated suppression in other murine tumor systems and the possible pivotal role for a tumor antigen-presenting cell in activating Ts3 in the S1509a tumor system [12].
• No age restriction was found for antigen presentation to Ts1 cells and for the interaction between Ts3 cells and target B cells [13].
• The data demonstrate that Ts3 induction is independent of the carrier requirements involved in helper T cell induction and is not dependent upon B cell priming [9].
• Anti-IJ mAb blocked Ts3 activation at the lymphocyte level whereas anti-IJ idiotype blocked activation at the accessory cell level [14].

Associations of Ts3 with chemical compounds

• Finally, we demonstrated that cyclophosphamide abrogates the suppressive effect of TsF2 but not that of Ts3 [12].

Other interactions of Ts3

• These three populations, termed Ts1, Ts2, and Ts3 have been characterized to have inducer, transducer and effector functions, respectively [15].
• It appears that antigen-activated CRI+ Ts3 require signals from the anti-CRI Ts2 subset to suppress DTH reactions in an idiotype-nonspecific manner [16].
• In contrast, the target of the Igh-V restriction of TsF2 appears to be the Ts3 cell, which carries antigen-specific, idiotype-related receptors [17].
• The present report analyzes the specificity of NP-specific Ts3 cells and factors derived from H-2 and Igh heterozygous (B6 X C3H)F1 mice [5].

Analytical, diagnostic and therapeutic context of Ts3

• The factors from three types of suppressor T cell hybridomas, each representing the immortalized analogues of the inducer T suppressor cell (Ts1), transducer suppressor cell (Ts2), and effector suppressor cell (Ts3) network populations, were tested [18].

References