Enhancement of LFA-1-mediated cell adhesion by triggering through CD2 or CD3 on T lymphocytes

Kooyk, Yvette van; Kemenade, P van de Wiel-van; Weder, Pauline; Kuijpers, TW; Figdor, Carl G.

doi:10.1038/342811a0

Cited by 441 publications

(287 citation statements)

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“…This explanation could account for the inhibition of CD3-mediated up-regulation of T cell adhesion but not that of LFA-l-mediated up-regulation. The latter is known not to depend upon a CD4-CD3/TcR interaction [15]. The present results are, thus, compatible with the hypo thesis that CD4 ligands and putative CD4 ligands (gpl60 and MHC class II-derived peptides) can inhibit through negative signaling of both activated and resting T cell adhesion ( [6,33,34]; Mazerolles et aL, Hum.…”

Section: Discussionsupporting

confidence: 91%

“…1A, incubation of resting CD4+ T lymphocytes with increasing concentrations of plastic- NKIL16 is a CD 1 la-specific antibody, known to enhance homotypicTcell adhesion and agrégation [15]. Our results indicate that a short incubation of CD4+ T cells with increasing concentrations of NKIL16 ( …”

Section: Up-regulation Of Cd4+ T Cell Adhesion By Anti-cd3 (Okt3) Andmentioning

confidence: 65%

“…This event is secondary to T cell activation and can thus not account for mediating early T cell adhesion associated with T cell activation [1,2]. Recently, Dustin and Springer [14] and Keizer et al [15] demonstrated that CD3 cross-linking may result in an early up-regulation of Tcell adhesion that relies on a transient increase in the affinity of LFA-1 for its ligand [16,17]. This event is thought to be mediated by a conformational change related to PKC phosphorylation of LFA-1 or of an associated protein [14,17].…”

Section: Introductionmentioning

confidence: 99%

“…This event is thought to be mediated by a conformational change related to PKC phosphorylation of LFA-1 or of an associated protein [14,17]. A more prolonged up-regulation of T cell adhesion can also be induced by an LFA-1-specific antibody, NKIL16, that may induce homotypic cell agregation [15].…”

Section: Introductionmentioning

confidence: 99%

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Regulation of LFA‐1‐mediated T cell adhesion by CD4

et al. 1991

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Heterotypic adhesion of T lymphocytes to monocytes, B lymphocytes, or other target cells is mainly mediated by LFA-1 and CD 2 molecules. Low-affinity binding of restingTcells can be transiently up-regulated by cross-linking of CD3. We have previously found that binding of specific ligands to CD4 can down-regulate adhesion of resting T cells to B cells. We now show that the enhanced adhesiveness of CD4+ T cells induced by CD3 cross-linking using plastic-bound anti-CD3 antibody can also be inhibited by several CD4 ligands, i.e. anti-CD4 antibodies, the gpl60 env protein of human immunodeficiency virus, as well as by putative CD4 ligands, i.e. synthetic peptides analogous to the gp 160-binding site to CD4 (positions 418-434 and 449-464) and a 12-mer synthetic peptide (DR-12) analogous to positions 35-46 of HLA class II |3 subunit and including the highly conserved Arg-Phe-Asp-Ser (RFDS) sequence» After CD3 cross-linking, maximal binding of Tcells to HLA class II-positive and -negative B cells was similar, although binding to HLA class II-negative B cells was more prolonged.Tcells that were passively induced to up-regulate adhesion by binding of a CD 1 la-specific antibody, NKIL16, known to enhance LFA-1-dependent adhesiveness, were less sensitive to the inhibitory effect of the DR-12 peptide, whereas the inhibitory effects of gpl60 were preserved. The kinetics of adhesion of NKIL16-pretreated T cells was not influenced by LILA class II expression at the B cell surface. Together, these results strongly suggest that CD4-HLA class II interaction may down-regulate low-affinity adhesion of resting T cells and, to some extent, high-affinity adhesion of T cells actively induced by CD3 cross-linking but not passively induced by an anti-CD 11a antibody 1 Introduction

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Section: Discussionsupporting

confidence: 91%

Section: Up-regulation Of Cd4+ T Cell Adhesion By Anti-cd3 (Okt3) Andmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of LFA‐1‐mediated T cell adhesion by CD4

et al. 1991

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“…The role of ICAM-1/LFA-1-mediated adhesion has been established as a critical event for strengthening the contact between DC and Th cells leading to optimal Th cells activation [39], Th1-differentiation [30] and cytotoxicity [40], among others. Besides, ICAM-1/LFA-1 interaction also controls NK cell functional responses [41].…”

Section: Discussionmentioning

confidence: 99%

NK cells from tuberculous pleurisy express high ICAM‐1 levels and exert stimulatory effect on local T cells

et al. 2009

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Tuberculous pleurisy, one of the most common manifestations of extrapulmonary tuberculosis, is characterized by a T-cell-mediated hypersensitivity reaction along with a Th1 immune profile. In this study, we investigated functional cross-talk among T and NK cells in human tuberculous pleurisy. We found that endogenously activated pleural fluidderived NK cells express high ICAM-1 levels and induce T-cell activation ex vivo through ICAM-1. Besides, upon in vitro stimulation with monokines and PAMP, resting peripheral blood NK cells increased ICAM-1 expression leading to cellular activation and Th1 polarization of autologous T cells. Furthermore, these effects were abolished by anti-ICAM-1 Ab. Hence, NK cells may contribute to the adaptive immune response by a direct cellcontact-dependent mechanism in the context of Mycobacterium tuberculosis infection.Key words: ICAM-1 . NK cells . Pleurisy . Th1 . Tuberculosis Supporting Information available online IntroductionPleuritis is the most frequent clinical manifestation of extrapulmonary tuberculosis (TB) among young adults, and is normally considered a relatively benign form of disease since it may resolve without chemotherapy [1]. Tuberculous pleurisy is caused by a severe delayed-type hypersensitivity reaction in response to the rupture of a subpleural focus of Mycobacterium tuberculosis (Mtb) infection, but it may also be developed as a complication of primary pulmonary TB [2,3]. This pleural effusion is characterized by a strong granulomatous inflammatory response to Mtb together with high levels of . NK cells are CD56 1 CD16 1/À /CD3 À CD19 À lymphocytes of the innate immune system whose function is controlled by an array of germline-encoded activator/inhibitory receptors [5,6]. Two subsets of NK cells have been identified in humans according to CD56 expression differing in phenotype and function, and also in terms of chemokine receptors and adhesion molecules expression [7,8,9]. Functionally, CD56 bright cells are effective cytokine producers, whereas CD56 dim cells are efficient effectors of natural and Ab-dependent target cell lysis. Recently, we have described that an endogenously activated pleural fluid NK (PF-NK) population is a major source of IFN-g in response to Mtb [10,11]. Consistently, PF-NK are enriched in CD56 bright cells, as has been observed in other chronic inflammatory sites [12,13] or in tumor-affected tissues [14]. Together with the classical NK functions (i.e. cytotoxicity and cytokine production), novel skills have recently been described in niche-specific and in vitro-activated human NK cells. These unconventional capabilities include [16,17,18] and direct pathogen recognition [19,20]. In this regard, a novel innate immune cell population called Interferon-producing killer dendritic cells has been recently described in mice [21,22].ICAM-1/CD54 is the major ligand of costimulatory a L b 2 integrin (CD11a/CD18), commonly known as lymphocyte function-associated antigen (LFA-1) [23,24]. The surface enhancement of ICAM-1 on endothelial, APC and...

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