A monoclonal antibody detecting an Ia specificity mapping in the I-A or I-E subregion

Symington, Frank W.; Sprent, Jonathan

doi:10.1007/bf00344299

Cited by 67 publications

(26 citation statements)

References 19 publications

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“…In the present study we asked whether known differences in the MHC specificity of various T-cell (22,23). In some cases, these cells were cultured for 6 days in the presence of concanavalin A (Con A) at 2 ,ug/ml and 50% mouse Con A supernatant before purification (see figure legends).…”

Section: Introductionmentioning

confidence: 99%

T-cell receptor variable region gene usage in T-cell populations.

Garman¹,

Ko²,

Vulpe³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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We have examined T-cell receptor alpha- and beta-chain variable (V) region gene usage in T-cell populations predicted to have different major histocompatibility complex-restriction specificities. Using a sensitive ribonuclease protection assay to measure T-cell receptor mRNA levels, we found no striking differences in the usage of three V alpha genes and three V beta genes in T-cell populations from three congeneic H-2-disparate strains of mice and between the mutually exclusive Ly2+ L3T4- and Ly2- L3T4+ T-cell subpopulations. These results suggest that major histocompatibility complex restriction cannot be explained by the differential usage of nonoverlapping V alpha or V beta gene pools. In contrast, striking but unpredictable differences were seen in V gene usage in populations of T cells selected by activation with particular alloantigens.

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Section: Introductionmentioning

confidence: 99%

T-cell receptor variable region gene usage in T-cell populations.

Garman¹,

Ko²,

Vulpe³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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“…Using normal splenic B cells, we found that the enhancing effects of the class 11-specific mAb 34-5-3s shown inTable 2 were also seen using two additional Apb-specific mAb (28-16-8s and BP107), although all three are of different isotypes of Ig (IgG2a, IgM and IgG3, respectively). The observation that BP107 provides the lowest enhancement may be due to its comparatively lower binding of Apb [15]. However, the class I-specific IgG2a mAb SF1-1.1.1 did not enhance B cell proliferation, either in the presence or absence of CD4OL (Table 3A, groups 3 and S), although this mAb binds well to H-2d splenocytes (J. Harty, unpublished data).…”

Section: Anti-class I Mab Do Not Enhance Cd40-mediated Signalsmentioning

confidence: 88%

“…The class 11-specific mAb used in these studies included the Ek-specific mAb 14-4-4s and 17-3-33 [13] and the Aphspecific mAb 34-5-3s 1141, 28-16-83 (141 and BP107 [15]. The non-mitogenic anti-IgM mAb used was Bet-2 [16].…”

Section: Antibodiesmentioning

confidence: 99%

Signaling via major histocompatibility complex class II molecules and antigen receptors enhances the B cell response to gp39/CD40 ligand

1995

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Activated T cells induce proliferation and differentiation of resting B cells in vitro through their CD40 molecules and lymphokine receptors. However, despite constitutive B cell expression of CD40 and lymphokine receptors, widespread nonspecific polyclonal B cell activation by activated T cells is seldom observed in vivo. The present study was designed to test the hypothesis that signals delivered via the B cell antigen (Ag) receptor (membrane immunoglobulin, mIg) and major histocompatibility complex (MHC) class II molecules enhance B cell responsiveness to CD40-mediated signals, providing specificity to the Ag-nonspecific, MHC-unrestricted CD40 signal. To test this hypothesis, both an Ag-specific mouse B cell clone CH12.LX, and freshly isolated resting splenic B cells were cultured with either soluble or membrane-bound forms of the T cell ligand for CD40 (CD40L), in the presence or absence of additional signals provided by Ag or anti-IgM, interleukin-4, and class II-specific monoclonal antibody (mAb). Differentiation of CH12.LX cells and proliferation of splenic B cells in response to both forms of CD40L was greatly enhanced by exposure to mIg-mediated signals, with greatest enhancement seen when cells were cultured with Ag prior to receiving other signals. Response to CD40L was further enhanced by concurrent culture with class II-specific, but not class I-specific mAb. Enhancement was greatest at limiting concentrations of CD40L. The ability of class II MHC-mediated signals to enhance Ag-specific B cell responsiveness to CD40-mediated signaling may selectively promote the activation of B cell clones capable of cognate interactions with helper T cells.

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“…Anti-TCRap-FITC (H57-597; [36]), anti-Thy-1-PE, and anti-CD44-PE (all from PharMingen, San Diego, CA), and anti-B220-FITC (Caltag, Burlingame, CA) were used for FACS analysis and cell sorting. Anti-MHC class I1 antibodies 28-16-83 [37] and BP109 [38], donkey anti-rat IgG and donkey anti-mouse IgG (Jackson ImmunoResearch Laboratories, West Grove, PA) were used for lymph node T cell purification. Primary and detection anti-IL-2 antibodies JES6-1A12 and JES6-5H4-biotin (PharMingen) were used for the IL-2 ELISA.…”

Section: Media and Reagentsmentioning

confidence: 99%

The role of tyrosine phosphorylation and PTP‐1C in CTLA‐4 signal transduction

Allison

1996

Eur J Immunol

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Recently, there has been increasing interest in the inhibitory regulators of lymphocyte activation, and in particular, the role of CD28 homologue CTLA-4 in the regulation of T cell responses. Interaction of CTLA-4 with B7 ligands inhibits T cell responses, including T cell proliferation and interleukin-2 (IL-2) secretion. The mechanism(s) responsible for CTLA-4 signal transduction are unknown, but it has been suggested that tyrosine phosphorylation is involved. Here we demonstrate that phorbol ester phorbol 12-myrislate 13-acetate (PMA), which increases tyrosine phosphorylation by stimulating protein kinase C and p21ras, can overcome the CTLA-4-mediated inhibition of T cell proliferation. This provides the first functional evidence that tyrosine phosphorylation is involved in CTLA-4 signal transduction. Most interestingly, CTLA-4-mediated inhibition of IL-2 secretion was not influenced by the presence of PMA. Further, we demonstrate that CTLA-4 cross-linking inhibits proliferation and IL-2 secretion of T cells from motheaten mice. These mice lack PTP-1C, a tyrosine phosphatase which mediates in a number of lymphocyte inhibitory responses, indicating that PTP-1C is not essential for CTLA-4 signaling. Collectively, these results demonstrate that regulation of tyrosine phosphorylation plays a pivotal role in CTLA-4 function, and that the inhibition of the transition from G0/G1 to the S phase of the cell cycle and the inhibition of IL-2 secretion require distinct signaling pathways. These experiments provide a useful model system which can be used to elucidate the signaling pathways involved in CTLA-4 function and to understand how CTLA-4, CD28 and Tcell receptor-mediated signals are integrated in T cell responses to antigen.

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A monoclonal antibody detecting an Ia specificity mapping in the I-A or I-E subregion

Cited by 67 publications

References 19 publications

T-cell receptor variable region gene usage in T-cell populations.

T-cell receptor variable region gene usage in T-cell populations.

Signaling via major histocompatibility complex class II molecules and antigen receptors enhances the B cell response to gp39/CD40 ligand

The role of tyrosine phosphorylation and PTP‐1C in CTLA‐4 signal transduction

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