Characterization of the Murine Antigenic Determinant, Designated L3T4a, Recognized by Monoclonal Antibody GK 1.5: Expression of L3T4a by Functional T Cell Clones Appears to Correlate Primarily with Class II MHC Antigen‐Reactivity

Dialynas, Deno P.; Wilde, D B; Marrack, Philippa; Pierrès, Anne; Wall, Kathleen; Havran, Wendy L.; Otten, Gillis R.; Loken, Michael R.; Pierres, Michel; Kappler, John W.; Fitch, Frank W.

doi:10.1111/j.1600-065x.1983.tb01083.x

Cited by 980 publications

(403 citation statements)

References 62 publications

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“…In addition, culture supernatants from a hybridoma producing anti-LFA-1 antibody were inhibitory in both systems. Unlike Lyt-2, LFA-1 expression is not correlated with class I or class II MHC recognition (8). Again, similar titration curves were obtained for these antibodies in the blocking of LDCC of H-2-positive and H-2-negative target cells.…”

Section: Blocking Of Ldcc Mediated By Polyclonally Induced Ctl With Asupporting

confidence: 68%

Monoclonal anti-Lyt-2.2 antibody blocks lectin-dependent cellular cytotoxicity of H-2-negative target cells.

Hünig¹

1984

The Journal of Experimental Medicine

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During the past years, a number of T cell antigens defined by conventional serology and monoclonal antibodies have become the basis for the distinction of T cell subsets, especially in the human, murine, and rat systems (reviewed in reference 1). Some of these markers have been directly correlated with T cell functions, either because they are only expressed on a given functional subset or because antibodies to them block or stimulate certain T cell reactions. A well studied example is the murine Lyt-2 (human OKT8/Leu-2) antigen. Originally thought to be a marker for cytotoxic (and suppressor) T cells (2), more recent data suggest an association of this antigen with T cell recognition of class I major histocompatibility complex (MHC) 1 antigens rather than with cytolytic function (3). Thus, Class I-specific helper T cells were found to be Lyt-2 + as well (4), and conversely, class II specific cytolytic T lymphocytes (CTL) with little or no Lyt-2 antigen were described (5). In the human, an analogous antigen is known to be associated with the recognition of class II MHC antigens (OKT4/Leu-3) (6, 7), and its likely murine counterpart (L3T4) has been described recently (8). The strongest evidence for an involvement of the molecules bearing these antigens in the recognition of MHC restriction elements is the capacity of antiLyt-2 (3) and anti-L3T4 (8) antibodies (and their counterparts in the human system [9]) to block the activities of cytotoxic and helper T cells that recognize class I and class II antigens, respectively. Accordingly, it has been proposed that the T cell structures defined by these antibodies interact with monomorphic determinants on MHC molecules, thereby providing an MHC class-specific recognition step in addition to the T cell receptors' interaction with its target antigen (3).Recently, evidence has been presented suggesting that the mechanism by which lectins polyclonally activate T cells (10) and mediate nonspecific (CTL)-lysis (1 1) (lectin-dependent cellular cytotoxicity, LDCC) is similar or identical to that operating in antigen-specific systems. Thus, it has been postulated that T ceils recognize lectin-modified MHC antigens on "accessory" and target cells. The finding that LDCC (12) and lectin-induced reactivity to interleukin 2 (IL-2) This work was supported by Sonderforschungsbereich 105, Wfirzburg. 1 Abbreviations used in this paper: CTL, cytotoxic T lymphocytes; Con A, concanavalin A; IL-2, interleukin 2; LDCC, lectin-dependent cellular cytotoxicity; LFA, lymphocyte-function associated antigen; MHC, major histocompatibility complex; NK, natural killer cells.J. ExP. MEn.

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Section: Blocking Of Ldcc Mediated By Polyclonally Induced Ctl With Asupporting

confidence: 68%

Monoclonal anti-Lyt-2.2 antibody blocks lectin-dependent cellular cytotoxicity of H-2-negative target cells.

Hünig¹

1984

The Journal of Experimental Medicine

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“…Polyclonal rabbit antimouse Ig was prepared by affinity purification on mouse Ig-Sepharose columns. mAbs GK1.5 (14) and 2B6 (15) (anti-CD4), 3.155 (anti-Lyt-2 (CD8)) (16), M1/70.15 (anti-MAC-1) (17), J11d.8 (anti-J11d) (18), HO13.4 (anti-Thy1.2) (19), Mar 18.5 and MARK-1 (anti-rat -chain) (20), and KJ1-26 (anti-DO11.10 clonotype) (13) were prepared from the supernatants of hybridoma cell lines, as previously described (21). Biotinylated anti-CD25 (mAb 3C7) and anti-CD69 (mAb H1.2F3) were purchased from BD PharMingen (San Diego, CA).…”

Section: Reagents and Absmentioning

confidence: 99%

Continued Antigen Stimulation Is Not Required During CD4+ T Cell Clonal Expansion

Lee

Pasos

Cecchini

et al. 2002

The Journal of Immunology

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Peptide Ag initiates CD4+ T cell proliferation, but the subsequent effects of Ag on clonal expansion are not fully known. In this study, murine CD4+ T cells were labeled with the fluorescent dye CFSE and were stimulated with specific peptide Ag. Activation occurred, as CFSE-associated fluorescence was reduced 2-fold with each cell division. Separation of proliferating cells based upon CFSE fluorescence intensity showed that daughter cells from each cell division proliferate even after removal of Ag. A limited exposure (∼2 h) to peptide programmed the cells to proliferate independently of Ag. Although not required for cell division, Ag increased the survival of proliferating cells and increased the total number of cell divisions in the expansion process. These results indicate that Ag exposure begins a program of cell division that does not require but is modified by further TCR stimulation.

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“…The following rat MoAbs were produced in ascitic form: GK1.5, an anti-CD4 IgG2b MoAb [21]; H35-17.2, an anti-CD8 IgG2b MoAb [22]; R46A2, a neutralizing anti-IFN-IgG1 MoAb [23]. As control, we used ascites of LO-DNP-2 hybridoma cells (kindly provided by Dr H. Bazin, Experimental Immunology Unit, Université Catholique de Louvain, Belgium), secreting a rat IgG1 MoAb with anti-DNP specificity.…”

Section: Moabs and Nitric Oxide Synthase Inhibitor Injected In Vivomentioning

confidence: 99%

Administration of anti-CD3 monoclonal antibody during experimental Chagas’ disease induces CD8+ cell-dependent lethal shock

Jacobs

Dubois

Carlier

et al. 1996

Clinical and Experimental Immunology

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SUMMARYThe injection of the 145-2C11 anti-CD3 MoAb in mice induces a polyclonal T cell activation resulting in the release of several cytokines, including interferon-gamma (IFN-) and tumour necrosis factoralpha (TNF-). As these cytokines are known to be involved in the host defence against Trypanosoma cruzi, we measured serum levels of IFN-and TNF-after injection of the 145-2C11 MoAb in the course of experimental murine Chagas' disease. Compared with control mice, T. cruzi-infected BALB/c mice were found to be primed to secrete very high levels of IFN-and TNF-from the second and the first week of infection, respectively, up to the chronic phase. In vivo cell depletion experiments indicated that CD8 T cells were responsible for these dramatic hyperproductions of IFN-and TNF-. While all control mice survived anti-CD3 MoAb injection, a high lethality rate was observed in T. cruzi-infected mice within 24 h after anti-CD3 MoAb challenge. Pretreatment with neutralizing anti-IFN-MoAb or depletion of CD8 T cell population dramatically decreased the mortality induced by anti-CD3 MoAb in T. cruzi-infected mice. Finally, we showed that anti-CD3 MoAb injection in T. cruzi-infected mice was followed by a massive release of nitric oxide (NO) metabolites, which was partially reduced by IFN-or TNF-neutralization. The administration of the NO synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) before anti-CD3 MoAb challenge did not prevent and even enhanced lethality in T. cruzi-infected mice, suggesting that NO overproduction and lethal shock are not causally related. We conclude that injection of anti-CD3 MoAb in the course of experimental Chagas' disease induces a CD8 cell-dependent shock mediated by IFN-and TNF-.

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Characterization of the Murine Antigenic Determinant, Designated L3T4a, Recognized by Monoclonal Antibody GK 1.5: Expression of L3T4a by Functional T Cell Clones Appears to Correlate Primarily with Class II MHC Antigen‐Reactivity

Cited by 980 publications

References 62 publications

Monoclonal anti-Lyt-2.2 antibody blocks lectin-dependent cellular cytotoxicity of H-2-negative target cells.

Monoclonal anti-Lyt-2.2 antibody blocks lectin-dependent cellular cytotoxicity of H-2-negative target cells.

Continued Antigen Stimulation Is Not Required During CD4+ T Cell Clonal Expansion

Administration of anti-CD3 monoclonal antibody during experimental Chagas’ disease induces CD8+ cell-dependent lethal shock

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