CD4+CD7-CD57+ T cells: a new T-lymphocyte subset expanded during human immunodeficiency virus infection

Legac, Éric; Autran, Brigitte; Merle‐Béral, Hélène; Katlama, Christine; Debré, Patrice

doi:10.1182/blood.v79.7.1746.1746

Cited by 83 publications

(23 citation statements)

References 27 publications

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“…Their proportions in the peripheral blood also increase in patients with colorectal cancer [6,7]. CD57 þ T cells reportedly increase in patients with AIDS [8,9] and those subjected to kidney, heart and bone marrow (BM) transplantation [10][11][12]. It is suggested that these T cells with NK cell markers may be counterparts of extrathymic T cells in mice [13], which have intermediate T cell receptor (TCR) (a major proportion also have NK cell marker, NK1.1), and contain potentially self-minor lymphocyte stimulatory (Mls) antigen-reactive clones [14,15] and thereby may play a role in inducing autoimmune diseases [14][15][16].…”

Section: Introductionmentioning

confidence: 95%

Increase of CD57+ T cells in knee joints and adjacent bone marrow of rheumatoid arthritis (RA) patients: implication for an anti-inflammatory role

Arai¹,

Yamamura²,

Seki³

et al. 1998

Clinical and Experimental Immunology

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The distribution of CD57+ T and CD56+ T cells in patients with RA was examined. In control osteoarthritis patients, these cells exist as a minor population in the peripheral blood. Our data show that in patients with RA, CD57+ T cell levels are elevated in peripheral blood, knee joint fluid, knee synovial membrane and bone marrow (BM), compared with peripheral blood of controls. CD57+ T cells are especially high in knee joint fluid and joint‐adjacent BM, while CD56+ T cells show no such increase. CD57+ T cells contain a major population of CD8+ cells and higher proportions of CD4−8− cells and γδ T cells than do CD57−T cells. CD57+T cells in peripheral blood and joint fluid increase with the duration of disease. Erythrocyte sedimentation rate (ESR) is inversely correlated with the proportion of CD57+T cells in the joint fluid. Although RA frequently occurrs in patients with CD3+57+ cell leukaemia, and some CD57+T cells are likely to be involved in the onset of RA, we suggest that CD57+T cells may rather suppress inflammation of RA, and other cellular components (e. g. granulocytes) may govern the severity of the inflammation of RA. These CD57+ T cells are probably generated extrathymically in the adjacent BM or joint space.

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Section: Introductionmentioning

confidence: 95%

Increase of CD57+ T cells in knee joints and adjacent bone marrow of rheumatoid arthritis (RA) patients: implication for an anti-inflammatory role

Arai¹,

Yamamura²,

Seki³

et al. 1998

Clinical and Experimental Immunology

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“…First, antibody cross-linking of CD7 induces an increase in intracellular calcium [ 131. Second, various studies have demonstrated both inhibitory and stimulatory effects of CD7-specific mAb on the proliferation and cytokine response of both a@+ Tcells and y/6+ Tcells [14-191. Furthermore, changes in CD7 expression on T cells or T cell subsets have been reported in various disease states, including HIV infection [20] and rheumatoid arthritis [21]. CD7 has also recently been implicated as a potential cofactor in syncytium formation induced by HIV-1 [22].…”

Section: [I 132681mentioning

confidence: 99%

Tyrosine kinase activity associated with the CD7 antigen: correlation with regulation of T cell integrin function

Chan¹,

Reynolds²,

Shimizu³

1994

Eur J Immunol

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Rapid up-regulation of the functional activity of integrin adhesion receptors is a hallmark of T cell activation. Monoclonal antibody engagement of the CD7 antigen on human T cells results in an increase in beta 1 and beta 2 integrin-mediated adhesion within minutes. This suggests that CD7 is capable of transducing intracellular signals, and is consistent with other indirect studies implicating CD7 as a signaling receptor on T cells. In this report, we have explored the intracellular mechanism by which CD7 modulates integrin functional activity. First, CD7-mediated up-regulation of T cell adhesion was found to be unique when compared to phorbol ester stimulation and CD3/T cell receptor cross-linking, based on differences in the kinetics of activation-dependent integrin-mediated adhesion and lack of increase in CD2 functional activity. Second, up-regulation of integrin activity mediated by CD7 cross-linking was completely inhibited by the tyrosine kinase inhibitor herbimycin A. Third, antiphosphotyrosine immunoblotting demonstrated that antibody engagement of CD7 results in a rapid but transient increase in tyrosine phosphorylation in human T cells. Finally, CD7 immunoprecipitates contain in vitro kinase activity, as demonstrated by phosphorylation of a predominant band of 80 kDa and multiple other bands. Phosphoamino acid analysis of the 80-kDa substrate revealed phosphorylation on tyrosine as well as serine and threonine residues. Together, our results suggest that CD7 is associated with tyrosine kinase activity and that this tyrosine kinase activity correlates with the ability of CD7 to regulate T cell integrin functional activity.

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“…Indeed, both genes share similar promoter regions and exonic organization (60). Although most human peripheral CD4 + T cells are CD7 + , several immunodeficiency states including HIV infection (61,62), allogeneic bone marrow transplantation (63), and immunosenescence (64) are associated with the expansion of CD4 + CD7 -T cells reminiscent of the increase in CD4 + CD90cells in MAIDS. Further investigations are required to determine whether cAMP is indeed involved in the human CD4 + CD7phenotype and whether PKA type I antagonists can be considered as potential therapeutic agents in these diseases.…”

Section: Discussionmentioning

confidence: 99%

Increased cAMP levels and protein kinase (PKA) type I activation in CD4+ T cells and B cells contribute to the retrovirus‐induced immunodeficiency of mice (MAIDS). A useful in vivo model for drug testing in PKA type I‐ induced immunodeficiency

Rahmouni¹,

Aandahl

Trebak³

et al. 2001

FASEB j.

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Murine AIDS (MAIDS) is characterized by a lymphoproliferative disease and a profound anergy, which involves mostly CD4 + T cells. To better define the mechanisms responsible for anergy, we measured cAMP concentrations in the different lymphocyte subsets of the infected mice. CD4 + T cells and B cells displayed a dramatic 10-to 30-fold increase of cAMP. cAMP was also significantly increased in CD8 + T cells, although to a far lesser extent. The unusual CD4 + CD90 -T cells, typical of MAIDS, were characterized by a much higher cAMP level than their CD90 + counterparts. T cells of the infected mice were much more sensitive to inhibition by the cAMP analogue 8-CPT-cAMP, which confirmed increased in vivo exposure to cAMP. In accordance with the increased cAMP levels, PKA type I was constitutively activated and its C subunit was translocated to the nucleus. Finally, the profound T-cell anergy associated with MAIDS could be reversed by treating T cells with a PKA type I-selective antagonist ex vivo. MAIDS could constitute a suitable model for the study of new pharmacological agents aimed at reversing the immunosuppressive effects of cAMP previously shown to be involved in several pathological states, including HIV infection and common variable immunodeficiency.

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CD4+CD7-CD57+ T cells: a new T-lymphocyte subset expanded during human immunodeficiency virus infection

Cited by 83 publications

References 27 publications

Increase of CD57+ T cells in knee joints and adjacent bone marrow of rheumatoid arthritis (RA) patients: implication for an anti-inflammatory role

Increase of CD57+ T cells in knee joints and adjacent bone marrow of rheumatoid arthritis (RA) patients: implication for an anti-inflammatory role

Tyrosine kinase activity associated with the CD7 antigen: correlation with regulation of T cell integrin function

Increased cAMP levels and protein kinase (PKA) type I activation in CD4+ T cells and B cells contribute to the retrovirus‐induced immunodeficiency of mice (MAIDS). A useful in vivo model for drug testing in PKA type I‐ induced immunodeficiency

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