Project description:Activation of peripheral T lymphocytes in the absence of pathogen induced inflammation or costimulatory signals results in tolerance. Two different tolerance mechanisms have been described, deletion and anergy. We recently demonstrated that an important variable which is responsible for the decision between anergy and deletion for CD8 T cells is the strength of signaling through the T cell receptor(Redmond and Sherman, Immunity 22:275,2005). However, it is not know what the downstream signals are that result in death(deletion) vs. survival(anergy)of the activated cells. Marth and co-workers have previously shown that CD8 T cell apoptosis under conditions similar to those that occur during tolerance in vivo may involve a change in protein glycosylation (Van Dyken et.al., Mol.Cell.Bio.27:1096,2007).In order to assess the role of protein glycosylation in the decision between deletion vs. anergy in immune tolerance, we have prepared purified TCR transgenic CD8 T cells stimulated in vivo using a strong antigenic signal (anergy conditions) or a weak antigenic signal (deletion conditions) with cognate antigen. We wish to assess transcriptional differences in genes involved in protein glycosylation in these 2 cell populations. The control population will be naive trangenic CD8 cells. Dr. Sherman's lab aims to assess the role of protein glycosylation in the decision between deletion vs. anergy in immune tolerance, they have prepared purified TCR transgenic CD8 T cells stimulated in vivo using a strong antigenic signal (anergy conditions) or a weak antigenic signal (deletion conditions) with cognate antigen. Dr. Sherman's lab wishes to assess transcriptional differences in genes involved in protein glycosylation in these 2 cell populations. Then control population will be naïve transgenic CD8 cells. RNA preparations of mouse CD8 T cells from the B10D2 strain with three different conditions (Naïve, Deleted, and Anergic) were sent to the Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv4 microarrays.

Project description:Activation of peripheral T lymphocytes in the absence of pathogen induced inflammation or costimulatory signals results in tolerance. Two different tolerance mechanisms have been described, deletion and anergy. We recently demonstrated that an important variable which is responsible for the decision between anergy and deletion for CD8 T cells is the strength of signaling through the T cell receptor(Redmond and Sherman, Immunity 22:275,2005). However, it is not know what the downstream signals are that result in death(deletion) vs. survival(anergy)of the activated cells. Marth and co-workers have previously shown that CD8 T cell apoptosis under conditions similar to those that occur during tolerance in vivo may involve a change in protein glycosylation (Van Dyken et.al., Mol.Cell.Bio.27:1096,2007).In order to assess the role of protein glycosylation in the decision between deletion vs.anergy in immune tolerance, we have prepared purified TCR transgenic CD8 T cells stimulated in vivo using a strong antigenic signal (anergy conditions) or a weak antigenic signal (deletion conditions) with cognate antigen. We wish to assess transcriptional differences in genes involved in protein glycosylation in these 2 cell populations. The control population will be naive trangenic CD8 cells. Dr. Sherman's lab aims to assess the role of protein glycosylation in the decision between deletion vs. anergy in immune tolerance, they have prepared purified TCR transgenic CD8 T cells stimulated in vivo using a strong antigenic signal (anergy conditions) or a weak antigenic signal (deletion conditions) with cognate antigen. Dr. Sherman's lab wishes to assess transcriptional differences in genes involved in protein glycosylation in these 2 cell populations. Then control population will be naïve transgenic CD8 cells. RNA preparations of mouse CD8 T cells from the B10D2 strain with three different conditions (Naïve, Deleted, and Anergic) were sent to the Microarray Core (E). The RNA was amplified, labeled, and hybridized to both the GLYCOv3 and Mouse 430A_2.0 microarrays.

Project description:Activation of peripheral T lymphocytes in the absence of pathogen induced inflammation or costimulatory signals results in tolerance. Two different tolerance mechanisms have been described, deletion and anergy. We recently demonstrated that an important variable which is responsible for the decision between anergy and deletion for CD8 T cells is the strength of signaling through the T cell receptor(Redmond and Sherman, Immunity 22:275,2005). However, it is not know what the downstream signals are that result in death(deletion) vs. survival(anergy)of the activated cells. Here we analysze additional conditions: 1) Wild Type mice were injected injected only once with a strain of vaccinia virus that express hemagglutinin from influenza; 2) BIM KO Clone 4 transgenic T cells were transferred into B10D2 mice then injected daily for 3 days with 1ug of KdHA peptide and sorted by flow cytometry according to their expression of CD8 and thy1.1; 3) Mice injected with 1 ug (deleted condition) of influenza hemaglutinin antigen (HA), 24 hours post injection CD8 T CL4 cells were sorted by flow cytometry (FacsARIA) and 4) WildType mice injected with 100 ug (anergic condition) of influenza hemaglutinin antigen (HA), 24 hours post injection CD8 T CL4 cells were sorted by flow cytometry (FacsARIA). Dr. Sherman's lab aims to assess the role of protein glycosylation in the decision between deletion vs. anergy in immune tolerance, they have prepared purified TCR transgenic CD8 T cells stimulated in vivo using a strong antigenic signal (anergy conditions) or a weak antigenic signal (deletion conditions) with cognate antigen. Dr. Sherman's lab wishes to assess transcriptional differences in genes involved in protein glycosylation in these 2 cell populations. Then control population will be naïve transgenic CD8 cells. RNA preparations of mouse CD8 T cells from the B10D2 strain with three different conditions (Naïve, Deleted, and Anergic) were sent to the Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv4 microarrays.

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