Acquired Resistance to Experimental Autoimmune Encephalomyelitis Is Independent of Vβ Usage

Johnson, Brian D.; Nardella, John P.; McConnell, Thomas J.; Mannie, Mark D.

doi:10.1006/cimm.1997.1143

Cited by 12 publications

(5 citation statements)

References 63 publications

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“…The CD4 ϩ GP2.E5/R1 and GP2.5F3 clones and the CD4 Ϫ GP2.4E5 and GP2.3H3.16 (referred to as 3H3 herein) clones were derived from rats sensitized with an emulsion of GPMBP/complete Freund's adjuvant (CFA) [6,7]. The R2.2F4 and R2.2C8 T cell clones were isolated from rats sensitized with synthetic peptide R72-86 in CFA [4,5]. The CONAL.8D9 clone was derived from Lewis rats immunized with conalbumin in CFA.…”

Section: Derivation and Culture Of Lewis Rat T Cell Linesmentioning

confidence: 99%

“…4) were tested for antigen-specific accumulation of surface I-A glycoproteins. The antigen specificity of these T cells has been characterized in previous studies [4][5][6][7]. GP2.3H3.16 (3H3) and GP2.4E5 T cells were CD4 Ϫ T cells that exhibited little or no proliferative reactivity to RMBP but exhibited prolonged antigen presentation after culture with RMBP [7].…”

Section: The Partial Agonist Rmbp Stimulates Expression Of I-a Glycopmentioning

confidence: 99%

“…GP2.5F3 and GP2.E5/R1 CD4 ϩ T cells exhibited 10-to 30-fold less proliferative reactivity to RMBP compared with GPMBP. These T cells recognized RMBP as an antagonist in the presence of an anti-CD4 mAb and also acquired long-lasting T-APC activity after culture with RMBP and an anti-CD4 mAb [5][6][7]. R2.2C8 and R2.2F4 represent encephalitogenic T cells that express equipotent proliferative reactivity to RMBP and GPMBP [4,5].…”

Section: The Partial Agonist Rmbp Stimulates Expression Of I-a Glycopmentioning

confidence: 99%

“…Likewise, T-helper cells specific for the dominant encephalitogenic 72-86 region of MBP exhibit high reactivity to GPMBP but vary substantially in reactivity to RMBP. Rare T cells showing high reactivity to RMBP exhibit potent pathogenic activity, whereas T cells exhibiting low levels of RMBP reactivity induce mild disease or lack pathogenic activity [4,5]. Many T cells that have low reactivity to the 72-86 RMBP sequence recognize RMBP as a mixed or partial agonist/antagonist [6,7].…”

Section: Introductionmentioning

confidence: 99%

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An autologous self-antigen differentially regulates expression of I-A glycoproteins and B7 costimulatory molecules on CD4− CD8− T helper cells

Walker

White

Nardella

et al. 1999

Journal of Leukocyte Biology

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During inflammation, T helper cells transiently express class II major histocompatibility complex (MHC) glycoproteins and present antigens to other T cells. To assess involvement of self-antigens in the generation of T cell antigen-presenting cell (T-APC) activity, rat (R) myelin basic protein (MBP) was used to stimulate a rat CD4-CD8- T cell clone. RMBP induced T cell surface expression of class II MHC glycoproteins and T-APC activity, although RMBP did not elicit interleukin (IL-2) production or proliferation. When added to culture with the strong agonist guinea pig (GP) MBP, RMBP acted as a partial antagonist and inhibited responses of IL-2 production, proliferation, and T cell expression of B7.1. RMBP did not, however, efficiently antagonize GPMBP-induced I-A expression on T cells. These findings indicate that the self-antigen RMBP specifically induces accumulation of I-A/peptide complexes at signaling thresholds that inhibit pathogenic autoimmune responses. Overall, this study suggests a role for self-antigens in the generation of B7-deficient T-APC activity as a mechanism of tolerance in experimental autoimmune encephalomyelitis.

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Section: Derivation and Culture Of Lewis Rat T Cell Linesmentioning

confidence: 99%

Section: The Partial Agonist Rmbp Stimulates Expression Of I-a Glycopmentioning

confidence: 99%

Section: The Partial Agonist Rmbp Stimulates Expression Of I-a Glycopmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

An autologous self-antigen differentially regulates expression of I-A glycoproteins and B7 costimulatory molecules on CD4− CD8− T helper cells

Walker

White

Nardella

et al. 1999

Journal of Leukocyte Biology

Self Cite

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“…Reverse transcription (RT)-PCR was performed as described [54]. RNA (1.0 pg) was reverse transcribed and cDNA was subjected to 25 cycles of PCR (94°C for 1 min, 60°C for 2 min, 72°C for 2 min).…”

Section: Rna Extraction and Rt-pcr Analysesmentioning

confidence: 99%

Antigen presentation by T cells: T cell receptor ligation promotes antigen acquisition from professional antigen‐presenting cells

1997

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The purpose of this study was to determine whether the clonotypic specificity of the T cell receptor influences the specificity of T cell-mediated antigen presentation. We have previously shown that myelin basic protein (MBP)-specific Lewis rat GP2.E5/R1 (R1) T cells cultured with antigen, irradiated syngeneic splenocytes (IrrSPL) and tolerogenic monoclonal antibody become highly effective antigen-presenting cells (APC). In the current studies, we investigated the transfer of specific (MBP) and unrelated (conalbumin) antigens from antigen-pulsed SPL to R1 T cells. R1 T cells cultured with IrrSPL that were pulsed simultaneously with both MBP and conalbumin acquired and presented both antigens to the appropriate T cell responders in a secondary assay. These results suggested a physical transfer of major histocompatibility complex (MHC)/peptide complexes from professional APC to R1 T cells. Transfer of conalbumin from professional APC to R1 T cells required specific recognition of MBP and was optimal when both conalbumin and MBP were presented on the same group of professional APC. Antigens transfer did not occur when allogeneic SPL were used as APC. The anti-I-A mAb OX6 inhibited antigen transfer but only when added during the initiation of culture. OX6 also inhibited antigen acquisition by R1-trans, a variant of the R1 T cell line which constitutively synthesizes high levels of I-A, from MBP-pulsed IrrSPL but blockade of I-A did not inhibit antigen acquisition when soluble MBP was added directly to the culture. Despite constitutive synthesis of I-A, R1-trans T cells did not acquire guinea pig MBP from pulsed allogeneic APC. These studies demonstrate that although T cells of a particular specificity can present unrelated antigens, the cognate interaction of the T cell antigen receptor with the appropriate antigen/self-MHC complex strongly promotes acquisition of these complexes from professional APC.

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Partial Agonism Elicits an Enduring Phase of T-Cell-Mediated Antigen Presentation

Mannie

White

Nardella

et al. 1998

Cellular Immunology

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Acquired Resistance to Experimental Autoimmune Encephalomyelitis Is Independent of Vβ Usage

Cited by 12 publications

References 63 publications

An autologous self-antigen differentially regulates expression of I-A glycoproteins and B7 costimulatory molecules on CD4− CD8− T helper cells

An autologous self-antigen differentially regulates expression of I-A glycoproteins and B7 costimulatory molecules on CD4− CD8− T helper cells

Antigen presentation by T cells: T cell receptor ligation promotes antigen acquisition from professional antigen‐presenting cells

Partial Agonism Elicits an Enduring Phase of T-Cell-Mediated Antigen Presentation

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