Disease relevance of Ts2

• It has been found that the ability of anti-idiotypic second-order T suppressor cells (Ts2) to inhibit T cell-dependent delayed-type hypersensitivity (DTH) responses depended upon the presence of cross-reactive-idiotype (CRI)-bearing T cells present in ABA-primed mice [1].
• Regulation of cell-mediated immunity in cryptococcosis. III. Characterization of second-order T suppressor cells (Ts2) [2].
• Moreover, the in vivo administration of a factor that is derived from a Ts1 functioning hybrid cell line induced a second set of suppressor cells (Ts2) that upon transfer to syngeneic ABA-primed mice were able to inhibit granuloma formation in the footpad, as well as in the gastrointestinal tract after challenge with ABA-BSA-PAB [3].
• Dengue type 2 virus (DV) induces two generations of T suppressor cells (Ts1 and Ts2) in murine spleen [4].
• Five hybridoma T cell lines were prepared by fusion of second order suppressor T cells (Ts2) with the BW5147 thymoma [5].

High impact information on Ts2

• GT-TsF1 generates second-order suppressor T cells (Ts2) in H-2a,d,k haplotype mice [6].
• Two distinct processes of inhibition involving both a direct effect on IL-2-driven proliferation of responder T cells, and induction of a second-order suppressor cell (Ts2) were described [7].
• The mechanism by which I-J restrictions were imposed on second-order suppressor cells (Ts2) was analyzed [8].
• The I-J phenotype of this factor-presenting population controls the H-2 restriction of the Ts2 cells [8].
• These results differentiated the direct responder cell effect of MLR-TsF from its Ts2 inductive capacity, and localized the defect in responder cell proliferation to events occurring subsequent to IL-2 binding [7].

Chemical compound and disease context of Ts2

• In dengue type 2 virus (DV)-infected mice, the virus-specific immunosuppression is mediated by a two-step mechanism: (1) induction of T suppressor cells (Ts1) by by virus to produce a suppressor factor (SF) which (2) stimulates another subpopulation of T cells (Ts2) to produce prostaglandin which finally mediates suppression [9].

Biological context of Ts2

• The Ts2 cells were detectable 6 days after Ts1 injection, were specific in suppressing the cryptococcal delayed-type hypersensitivity (DTH) response, were T cells with an Lyt-1-,2+,Ia+ (I-J+) phenotype, were effective only on the efferent limb of the cryptococcal DTH response, and mediated their activity via a soluble factor (TsF2) [2].
• This is in marked contrast to TsF2 (derived from Id-specific Ts2-containing spleen cells), which lost its suppressive activity after reduction and alkylation, and behaves as a two chain factor after adsorption and elution from anti-I-J-coupled beads in the presence of DTT [10].
• Finally, we show that when Ts1-bearing mice are primed and boosted for anti-TMA antibody formation, the resulting response was overall reduced with respect to the idiotype-positive and negative plaque-forming cells that differs from the Ts2-bearing hosts wherein the idiotypic component is preferentially suppressed [11].

Anatomical context of Ts2

• Azobenzenearsonate (ABA)-specific T cell-derived suppressor factor (TsF1) from A/J mice was used to induced second-order suppressor T cells (Ts2) [12].
• Despite the absence of B cells in these cultures, the mature Ts2 cells were functionally IgH restricted [13].
• Injection of this TsF into naive A/J mice elicits a second set of specific suppressor cells (Ts2) which are not lysed by anti-CRI antibody plus C, and which do not bind to ABA-BSA-coated dishes [14].
• The data are discussed in terms of the nature of the determinants recognized by these antibodies as well as the potential uses of these reagents for studying the suppressor T cell pathway and potential relationships between Ts1, Ts2, and T helper cells [15].
• Briefly, cryptococcal antigen induces afferent suppressor and/or suppressor inducer (Ts1) cells in the lymph nodes of mice, and the Ts1 cells, or a soluble factor derived therefrom (TsF1), stimulate the production of second-order or efferent suppressor (Ts2) cells [2].

Associations of Ts2 with chemical compounds

• This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction [2].

Regulatory relationships of Ts2

• We demonstrated previously that S1509a-induced Ts1, TsF1, and Ts2 specifically suppress in vivo Ly1+2- T cell-dependent responses to S1509a and that Ts1 suppress in vivo Ly-1+2- T cell-mediated proliferative responses to S1509a [16].

Other interactions of Ts2

• Culture of naive C57BL/6 spleen cells with Ts1-derived suppressor factor in the absence of exogenous Ag leads to the generation of Ts2 cells that mediate Ag-specific suppression of NP plaque-forming cell responses [13].
• It appears that antigen-activated CRI+ Ts3 require signals from the anti-CRI Ts2 subset to suppress DTH reactions in an idiotype-nonspecific manner [1].
• Clonal analysis of regulatory cells revealed 2 populations of helper (Th1 and Th2) and suppressor (Ts1 and Ts2) T cells in spleen cells (SC) of tolerized mice [17].
• Neither deficiency in TNP-specific help nor dominance of TNP-specific suppression is involved in maintainance of tolerance, but tolerance appears to be sustained by interference of TNP-specific regulatory cells with anti-idiotypic regulatory cells (Th2, Ts2) [17].
• Our studies demonstrate that soluble proteins expressed by Ts2 cells (TsF2) specifically abrogate the DTH, cytotoxic, and nephritogenic potential of M52 cells, although T cell receptor and IL-2 receptor expression are unchanged in these unresponsive M52 clones [18].

Analytical, diagnostic and therapeutic context of Ts2

• The present study characterizes the cellular events that lead to the induction of the Ts2, suppressor transducer population [13].
• This latter point is in marked contrast to our previous observation that the tyr(TMA)-induced anti-idiotypic Ts2 fail to function intrinsically and can only be detected upon adoptive transfer into naive mice [11].
• By employing the in vitro culture technique, we demonstrated that the precursors of the functional Ts2 cells were L3T4- Lyt-1-2+ I-J- cells [19].
• A single intraperitoneal injection of the monovalent synthetic antigen, tyrosinated trimethylaminoaniline [tyr(TMA)] in Freund's complete adjuvant induces an antiidiotypic second-order T suppressor (Ts2) cell population 6 wk later [20].
• The fine specificity of anti-idiotypic, effector-phase suppressor T cells (Ts2) induced by the intravenous injection of syngeneic spleen cells covalently coupled with the 4-hydroxy-3-nitrophenyl acetyl (NP) hapten was studied in an in vitro plaque-forming cell system [21].

References