Superantigens related to B cell hyperplasia

Ponzio, Nicholas M.; Tsiagbe, V. K.; Thorbecke, G. J.

doi:10.1007/bf01795130

Cited by 9 publications

(5 citation statements)

References 150 publications

(100 reference statements)

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“…These lymphomas start in germinal centers (GCs) and express an Mtv29-encoded vSAg which strongly stimulates syngeneic V16+CD4 T cells. Thus, the observation in the present study that, in the presence of vSAg responsive T cells, vSAg expressed on B cells can induce GC formation, strongly supports the suggestion that vSAg expression on normal GC cells in SJL mice may cause abnormally vigorous GC production, possibly creating a condition permissive for lymphoma formation (Tsiagbe et al, 1998, Ponzio et al, 1996.…”

Section: Control-ig Tnf-r-igsupporting

confidence: 88%

Induction of Germinal Centers by MMTV EncodedSuperantigen on B Cells

Simmons

Simms

Chiarle

et al. 2001

Journal of Immunology Research

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It has not been established whether an endogenous superantigen (SAg) expressed on B cells can induce germinal centers (GCs). An interesting model is that of mammary tumor virus encoded viral SAgs, which induce vigorous T cell proliferation and are predominantly expressed on activated B cells. We have used this model to analyze the possibility that direct stimulation of Mtv7+ DBA/2 B cells by vSAg-responsive (Vβ6+) BALB/c T cells can give rise to GCs. Injection of BALB/c SCID mice iv with 2 × 106 DBA/2 B cells, together with LPS, followed by 2 × 106 BALB/c T cells induces numerous large splenic GCs within 3–5 days. The GCs are still large on day 7, but are very much reduced by day 10. B cell activation with LPS is needed for this effect. These GCs form in spite of the apparent absence of follicular dendritic cells (FDCs) as judged by staining for several FDC surface markers. Control mice receiving either BALB/c T or DBA/2 B cells + LPS alone or DBA/2 T + B cells + LPS fail to exhibit any GCs on days 3–7. Numerous small clusters of PNA+ cells, but few large GCs are observed when TNF-R(p55)-Ig is also injected, whereas LTβR-Ig treatment impeded the formation of aggregations of these cells even further, leaving scattered PNA+ single cells and very small clumps throughout the white pulp of the spleens. Anti-TNFα had no effect. These results suggest that endogenous vSAg mediated GC formation is independent of antigen trapping by FDCs.

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Section: Control-ig Tnf-r-igsupporting

confidence: 88%

Induction of Germinal Centers by MMTV EncodedSuperantigen on B Cells

Simmons

Simms

Chiarle

et al. 2001

Journal of Immunology Research

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“…T cell proliferation to nominal Ag presentation is IL-2 dependent, and NFAT is important for the production of IL-2 (15). Therefore, we also determined whether the addition of cyclosporin A (CSA), 4 an inhibitor of NFAT, to cultures of tumor-stimulated spleen cells blocked T cell proliferation (16). As shown in Fig.…”

Section: Nfat-dependent Division and Il-12-dependent Cytotoxicity Of mentioning

confidence: 99%

Tim-3+ T-bet+ Tumor-Specific Th1 Cells Colocalize with and Inhibit Development and Growth of Murine Neoplasms

Simmons

Koneru

Mohindru

et al. 2005

The Journal of Immunology

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Although T cells infiltrate many types of murine and human neoplasms, in many instances tumor-specific cytotoxicity is not observed. Strategies to stimulate CTL-mediated antitumor immunity have included in vitro stimulation and/or genetic engineering of T cells, followed by adoptive transfer into tumor-bearing hosts. In this model of B cell lymphoma in SJL/J mice, we used Tim-3+ T-bet+ Th1 cells to facilitate the development of tumor-specific CTL. Tumor-specific Th1 cell lines were polarized with IL-12 during in vitro stimulation and long term maintenance. As few as 5 million Tim-3+ T-bet+ Th1 cells enabled recipients to resist growth of malignant transplantable cells. In addition, similar numbers of Th1 cells injected into 2- to 3-mo-old mice inhibited development of the spontaneous primary lymphomas, which normally arise in 90% of aging mice. CFSE+ Th1 cells colocalized with injected tumor cells in vivo and formed conjugates with the tumor cells within follicles, whereas in nontumor-challenged recipients the CFSE+ Th1 cells localized only within the T cell zones of the spleen. These results provide evidence that adoptive immunotherapy with Tim-3+ T-bet+ tumor-specific Th1 cells can be used to induce host cytotoxic responses that inhibit the development and growth of neoplastic cells.

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“…passage of 10 6 -10 7 tumor cells (6-10 days post tumor transfer) into 6-10 week old syngeneic recipient mice. An in vitro RCS tumor cell line [34] was derived from the in vivo RCS tumor cell line, and maintained in culture with Iscove's modification of Dulbecco's medium (Cellgro; Mediatech; Herndon, VA) supplemented with 10% FCS (Cellgro), 1 mM Oxalacetic Acid, 1 mM Sodium Pyruvate, Insulin (20 Units/ml), nonessential amino acids, 2 mM L-glutamine/penicillin/streptomycin (all from Sigma; St. Louis, MO), and 0.05 mM 2-mercaptoethanol.…”

Section: Mice and Tumor Cellsmentioning

confidence: 99%

“…51 Cr release assay A 51 Cr release assay was used to determine levels of cytotoxic activity as previously described [9,40]. cNJ117 was the CTL-susceptible SJL tumor cell line used as a target in 51 Cr release assays [34]. cNJ117 was derived from the in vivo RCS tumor cell line, and both cell lines express the same surface antigens and stimulate similar host immune responses.…”

Section: Generation Of Cytotoxic Effector Cellsmentioning

confidence: 99%