Disease relevance of Ts1

• 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) [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].
• Dengue type 2 virus (DV) induces two generations of T suppressor cells (Ts1 and Ts2) in murine spleen [3].
• Japanese encephalitis virus (JEV) infection induces suppressor T-cells (Ts1) which suppress both the humoral (Ts-PFC) and cell mediated (Ts-DTH) immune response by producing soluble suppressor factors [4].
• In that work, we demonstrated that an i.v. injection of cryptococcal antigen (CneF) into CBA/J mice, to simulate the antigenemia known to occur in human cryptococcosis, induced a population of T suppressor cells (Ts1) in the lymph nodes (LN) [5].

High impact information on Ts1

• BALB/c mice immunized intravenously with syngeneic splenocytes, to which affinity-purified IgA produced by the MOPC 315 myeloma is covalently coupled, develop suppressor T cells (Ts1) that inhibit IgA secretion by MOPC 315 cells after 3-4 d of co-culture [6].
• However, in contrast with Ts1, these Ts2 do bind to plates bearing CRI+ anti-ABA immunoglobulin [7].
• Two-dimensional protein patterns from whole mouse embryos with different trisomies (Ts) (Ts1, -12, -14, -19) and from different organs (normal or malformed) and developmental stages of Ts12 embryos were analyzed by comparison with control patterns [8].
• Eight different Ts cell hybridomas (including inducer (Ts1) and effector (Ts3) suppressor cells) specific for the 4-hydroxy-3-nitrophenyl acetyl (NP) hapten were tested for their ability to respond to Ag or anti-CD3 antibody in a growth-inhibition assay [9].
• Results presented in this report demonstrate that all the Ts1 hybridomas described here express CD3-associated TCR-alpha beta [10].

Chemical compound and disease context of Ts1

• 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 [11].
• The suppressor cells in this model were shown to be T lymphocytes, which exerted their effect on the afferent limb of the DTH response; therefore, they were similar to the Ts1 cell in the ABA-DTH, NP-DTH, and NP cutaneous sensitivity models and to the afferent suppressor cells in the DNFB contact sensitivity system [12].
• We have previously shown that phenyltrimethylammonium (TMA)-specific, first-order suppressor T cells (Ts1) and soluble factors extracted from these cells (TsF1) can suppress delayed-type hypersensitivity (DTH) responses [13].

Biological context of Ts1

• 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 [14].
• No age restriction was found for antigen presentation to Ts1 cells and for the interaction between Ts3 cells and target B cells [15].
• Regulation of cell-mediated immunity in cryptococcosis. II. Characterization of first-order T suppressor cells (Ts1) and induction of second-order suppressor cells [5].
• The data further demonstrate that the idiotype-related determinants expressed on NP-specific Ts1 are controlled not by the Ighn genotype of the T cell donor, but by the genotype of the C57BL nu/nu (Ighb) recipient host [16].

Anatomical context of Ts1

• Administration of azobenzenearsonate (ABA)-coupled syngeneic spleen cells intravenously to A/J mice leads to the generation of suppressor T cells (Ts1) which exhibit specific binding to ABA-bovine serum albumin (BSA)-coated dishes [7].
• Further, both Early and Late Gm were able to generate NP-specific induction-phase suppressor cells (Ts1) when as few as 10(2) NP-coupled Gm were given i.v., the same as NP-SAC controls [2].
• The ability of an azobenzenearsonate (ABA)-specific suppressor T cell factor, a soluble extract from first order suppressor T cells (Ts1), and suppressor molecules produced by a long-term T cell hybridoma to regulate ABA-specific granuloma formation was studied [17].
• 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 [1].
• 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 [18].

Associations of Ts1 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 [1].

Regulatory relationships of Ts1

• 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 [19].

Other interactions of Ts1

• 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 [20].
• Previously published data have also been reinterpreted and another gene Ts-1 is shown to be associated with The A beta locus [21].
• These three populations, termed Ts1, Ts2, and Ts3 have been characterized to have inducer, transducer and effector functions, respectively [20].
• The cellular defect in Ts1 induction is controlled by the lpr gene, since age-matched congenic B6 mice do not display this defect [22].
• The antigen-presenting defect in the B6.lpr splenic adherent population for Ts1 induction is reversible by culturing the cells in interferon-gamma [22].

Analytical, diagnostic and therapeutic context of Ts1

• The in vitro culture technique will allow for further detailed studies of the interactions between the various cell populations and the Ts1 cell-derived soluble factor during the induction of Ts2 cells [23].
• Upon adoptive transfer, the Ts1 cells specifically suppressed the afferent limb of the delayed-type hypersensitivity (DTH) response to cryptococcal antigen [5].

References