Models for recognition of virally modified cells by immune thymus-derived lymphocytes

Doherty, Peter C.; Götze, Dietrich; Trinchieri, Giorgio; Zinkernagel, Rolf M.

doi:10.1007/bf01576981

Cited by 115 publications

(47 citation statements)

References 25 publications

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“…Perhaps the search for T-cell-mediated mechanisms allowing recovery from potentially lethal viral infections, such as ectromelia infection in mice (4) is a part of this evolutionary process. This idea is supported by findings that virus-immune cytotoxic T (T~) cells that specifically lyse virus-infected target cells in vitro (reviewed in reference 5), and promote recovery from primary viral infection in vivo (4) recognize H-2 antigens together with virus-specific antigens on infected cell surfaces (4)(5)(6)(7)(8)(9)(10)(11). The relevant genes in the H-2 complex map in either the K or the D region, but not in the I region (4,5,10,12,13).…”

mentioning

confidence: 66%

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

Blanden¹,

McKenzie²,

Kees³

et al. 1977

The Journal of Experimental Medicine

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The T(c)-cell response to ectromelia virus infection was studied in BALB/c-H-2(db) mice which carry a loss mutation in the H-2D region that results in the absence from cell surfaces of a molecule (D') bearing certain public H-2 specificities. When infected, these mice showed a poor response of T(c) cells that recognize H-2D(d) plus virus-specific determinants on infected macrophage targets, but gave a normal response to H-2K d plus virus-specific antigens. However, their own infected macrophages do display wild-type antigenic patterns involving virus and H-2D(d) since they were killed as efficiently as wild-type (BALB/c,H- 2(d))-infected cells by T(c) cells specific only for H-2D(d) plus viral antigens. When tested in vitro, infected BALB/c-H-2(db) cells stimulated a poor T(c)-cell response to H-2D plus virus-specific antigens, but stimulated a normal response (in comparison with infected BALB/c macrophages) to H-2K(d) plus viral antigens. Uninfected BALB/c-H-2(db) cells stimulated a normal T(c)-cell response to minor H antigens or trinitrophenyl in association with H-2D(d), thus suggesting that the defective response to infection may reside in a failure of the relevant H-2D(d) antigens of mutant cells to physically associate with viral antigens. Close association of viral and H-2D-coded molecules was also suggested by ability of specific anti-H-2K or -H-2D to partially block T(c)-cell-mediated lysis of infected targets. These results were interpreted to mean that H-2Dd-dependent, virus- immune T(c) cells recognized an antigenic pattern consisting of virus- specific and H-2D(d) determinants with the latter borne on an H-2D molecule carrying serologically-defined H-2D(d) private specificities. A second H-2D(d)-coded molecule (D') was not required for recognition and lysis by activated T(c) cells, but was apparently necessary for efficient stimulation of precursor T(c) cells, perhaps by promoting appropriate physical association of viral and H-2D(d) molecules.

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mentioning

confidence: 66%

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

Blanden¹,

McKenzie²,

Kees³

et al. 1977

The Journal of Experimental Medicine

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“…Thus, H-2 restriction is seen in both the primary lytic and the secondary induction phases. The same kind of restriction has been described in cell-mediated immunity to viral antigens (3). Two models have been proposed to account for this discriminant specificity of T cell recognition (1,3).…”

mentioning

confidence: 68%

“…The same kind of restriction has been described in cell-mediated immunity to viral antigens (3). Two models have been proposed to account for this discriminant specificity of T cell recognition (1,3). One model is that effector T cells have a single receptor that recognizes a single type of molecule, hapten-conjugated H-2 molecules or hybrid molecules of H-2 and viral antigens ("altered self").…”

mentioning

confidence: 89%

Specificity of memory cells raised against trinitrophenyl-conjugated syngeneic cells

Maeda¹,

McConnell²

1979

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

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Exogenous lipid analogues can be incorporated into purified plasma membranes of EL4 tumor cells. When EL4 membranes are incubated with sonicated ipid vesicles containing spin-labeled phosphatidylcholine and then purified, they exhibit paramagnetic resonance spectra characteristic of spin labels dilutely dispersed in the lipid bilayer. Also, when EL4 membranes are incubated with vesicles of fluorescent lipid (N-4-nitrobenzo-2-oxa-1,3-diazole phosphatidylethanolamine), the fluorescence intensity of the mixture gradually increases and the labeled membranes are strongly fluorescent under a microscope, whereas the original lipid vesicles are much less fluorescent because of self-quenching at the high relative concentration of the fluorophore in the vesicles (

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“…However, whether such recognition by T cells is mediated by two configurationally separated structures of recognition unit(s) (dual recognition) (8) or by a single continuously provided structure of recognition unit of T cells (modified self) (17) is, in spite of recent progress of molecular studies on T cell receptors (7), still unclear. Both of these arguments stand, although being considerably modified from their original forms.…”

Section: Discussionmentioning

confidence: 99%

Antigen‐Specific T Cell Cluster Formation on Antigen‐Pulsed Macrophage Monolayers in Mice

Saizawa

Mabuchi

Yokomuro

et al. 1987

Microbiology and Immunology

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We describe the quantitative measurement of antigen-specific clusters formed by antigen-pulsed macrophages and immunized T cells in mice. We have found the peripheral blood T cells show very little non-specific adhesion to macrophages in mice. By using this population of lymphocytes in the peripheral blood as the source of immunized T cells, we could quantitate antigen-specific cluster formation. On OVA-pulsed monolayers of peritoneal exudate macrophages from normal BALB/c mice, syngeneic peripheral blood T cells from donors immunized with the same antigen develop 20-40 clusters per 1,000 macrophages, whereas the same T cells on non-pulsed monolayers develop only 0-5 cluster-like accumulations of cells. On antigen-pulsed monolayers of macrophages from allogeneic (C57BL/6 or A/J) mice, clusters are developed only in the negative range (0-5/1,000 macrophages). Considering the observation by Braendstrup et al, these data seem to suggest that histocompatibility between macrophages and T cells is required to develop antigen-specific T cell clusters on antigen-pulsed macrophage monolayers, and that the genetic restriction of immune responsiveness may be directly expressed in this initial form of cellular interaction between antigen-bearing macrophages and specific T cells.

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Models for recognition of virally modified cells by immune thymus-derived lymphocytes

Cited by 115 publications

References 25 publications

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

Specificity of memory cells raised against trinitrophenyl-conjugated syngeneic cells

Antigen‐Specific T Cell Cluster Formation on Antigen‐Pulsed Macrophage Monolayers in Mice

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