Antigen recognition by T cells activated in the mixed lymphocyte reaction: specific binding of allogeneic cell material after removal of surface‐bound antigen by trypsin

Elliott, B. E.; Nagy, Zoltán Á.; Nabholz, Markus; Pernis, Benvenuto

doi:10.1002/eji.1830070509

Cited by 35 publications

(32 citation statements)

References 10 publications

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“…Hence, for absorption of shed molecules from APC, the much stronger absorption by activated than resting T cells could be largely a reflection of enhanced LFA-1-ICAM-1 interaction by activated T cells. Note that T cell absorption of shed molecules from APC has a precedent in the old observation that T cells activated to MHC alloantigens were able to absorb these Ags from APC sonicates (33,34).…”

Section: Discussionmentioning

confidence: 99%

Role of the Actin Cytoskeleton in T Cell Absorption and Internalization of Ligands from APC

Hwang

Sprent

2001

The Journal of Immunology

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A feature of T-APC interaction is that, via either TCR or CD28, T cells can absorb molecules from APC on to the cell surface and then internalize these molecules. Here, using both normal and TCR-transgenic T cells, we investigated the mechanism of T cell absorption of molecules from APC and the role of the cytoskeleton. The results show that although activated T cells could absorb APC molecules in the form of cell fragments, uptake of molecules by resting T cells required direct T-APC interaction. Based on studies with latrunculin B, surface absorption of molecules by resting T cells was crucially dependent upon the actin cytoskeleton for both CD28- and TCR-mediated absorption. Significantly, however, TCR-mediated absorption became strongly resistant to latrunculin B when the concentration of MHC-bound peptide on APC was raised to a high level, implying that the actin cytoskeleton is only important for absorption when the density of receptor/ligand interaction is low. By contrast, in all situations tested, the actin cytoskeleton played a decisive role in controlling T cell internalization of ligands from the cell surface.

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Section: Discussionmentioning

confidence: 99%

Role of the Actin Cytoskeleton in T Cell Absorption and Internalization of Ligands from APC

Hwang

Sprent

2001

The Journal of Immunology

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“…(2), we were unable to detect alloantigen on CTL grown in medium containing SCIF (Table VI) . Because trypsin treatment of primary MLCderived CTL removes receptor-bound alloantigen (22) and because trypsin-treated alloimmune T cells responded to SCIF as did untreated cells (Table VI), we are left with the conclusion that in the absence of alloantigen (signal 1) the nonspecific signal 2 (SCIF) provided by Lyl + T cells can trigger cell proliferation and secondary CTL responses within alloimmune LY2 .3+ T cells in an apparently autonomous fashion .…”

Section: Discussionmentioning

confidence: 99%

“…Following the procedure of Elliot et al . (22) MLC primed T cells were washed twice in PBS, pH 7 .4 without serum, and resuspended in PBS at a concentration of 2 X 107 cells/ml ; to 0 .5 ml of the cell suspension an equal volume of PBS containing trypsin (5 mg/ml) (trypsin T 1005, Sigma Chemical Co .) was added, and the mixture was incubated at 37'C for 30 min .…”

Section: Inhibition Of Dna-synthesismentioning

confidence: 99%

T-T-cell interactions during the vitro cytotoxic allograft responses. I. Soluble products from activated Lyl+ T cells trigger autonomously antigen-primed Ly23+ T cells to cell proliferation and cytolytic activity.

Wagner¹,

Röllinghoff²

1978

The Journal of Experimental Medicine

308

103

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Secondary murine cytotoxic T lymphocyte responses from alloantigen-primed T cells can be induced in vitro by apparently unrelated regimens, such as addition of either concanavalin A (Con A), conditioned medium from Con A stimulated lymphocyte cultures, conditioned medium from secondary mixed lymphocyte cultures (MLC), or stimulator cells sharing only the I-region with the stimulating cells used for primary sensitization. We now report that upon polyclonal (Con A), or antigen-specific (MLC) stimulation, Lyl+ T cells release a factor, which in turn triggers alloantigen primed Ly23+ T cells to proliferation and cytolytic activity. The secondary cytotoxic T lymphocyte inducing factor (SCIF) is produced within 24 h. For its production, an intact protein metabolism, not DNA metabolism, is required. Once induced, the functional activity of SCIF is nonspecific and not H-2 restricted. SCIF allows exponential growth and long-term propagation of cytolytic Ly23+ T cells with specificity to alloantigens used for primary sensitization. SCIF induced activation of alloantigen primed Ly23+ T cells does not require the presence of alloantigens. The results therefore reveal a process by which Lyl+ T-cell-derived nonspecific factor(s) induce autonomously Ly23+ T-cell-mediated, antigen-specific, cytotoxic T lymphocyte responses.

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“…As the suppression of immune reactivity was selective only affecting reactivity against the expected histocompatibility antigens, only two possible T-cell functions for specificity were deemed possible: according to our first alternative, there existed autoanti-idiotypic T cells functioning in a specific suppressive manner against the idiotypic-positive, anti-alloantigenreactive cells. A second alternative would be that soluble alloantigens derived from the original stimulator cells could be around on the surface of the MLC T blasts used for autoimmunization (8,14) in such a way as to lead to induction of alloantigen-specific suppressor T cells.…”

Section: Discussionmentioning

confidence: 99%

Induction of specific immune unresponsiveness with purified mixed leukocyte culture-activated T lymphoblasts as autoimmunogen. III. Proof for the existence of autoanti-idiotypic killer T cells and transfer of suppression to normal syngeneic recipients by T or B lymphocytes.

Binz¹,

Wigzell²

1978

The Journal of Experimental Medicine

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Specific immune unresponsiveness against a given set of histocompatibility antigens can be induced by immunization with autologous, antigen-specific T lymphoblasts. Such unresponsiveness can be transferred by lymphoid cells from autoblast-immunized donors to normal syngeneic recipients. The cells being most efficient in transferring the selective suppression are T lymphocytes from the spleen, especially if of Ly 1-2+3+ phenotype. By using such T lymphocytes we deem it likely that the actual underlying mechanism is one of actual transfer of autoanti-idiotypic killer T cells. In support for this view is the fact that such T cells endowed with exquisite specific, cytolytic reactivity towards autologous idiotype-positive T target cells exist in autoblast immune animals. Significant suppression may also be transferred with T cells of Ly 1+2-3- phenotype or with B cells. Here, we consider the suppressive mechanism to be one of production of autoanti-idiotypic antibodies. By using affinity fraction procedures, it was finally possible to prove that all T-cell suppressive activity resides in a population with true antigen-binding-specific receptors for the relevant idiotypes.

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Antigen recognition by T cells activated in the mixed lymphocyte reaction: specific binding of allogeneic cell material after removal of surface‐bound antigen by trypsin

Cited by 35 publications

References 10 publications

Role of the Actin Cytoskeleton in T Cell Absorption and Internalization of Ligands from APC

Role of the Actin Cytoskeleton in T Cell Absorption and Internalization of Ligands from APC

T-T-cell interactions during the vitro cytotoxic allograft responses. I. Soluble products from activated Lyl+ T cells trigger autonomously antigen-primed Ly23+ T cells to cell proliferation and cytolytic activity.

Induction of specific immune unresponsiveness with purified mixed leukocyte culture-activated T lymphoblasts as autoimmunogen. III. Proof for the existence of autoanti-idiotypic killer T cells and transfer of suppression to normal syngeneic recipients by T or B lymphocytes.

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