Back to the future –defining NK cells and T cells

Lanier, Lewis L.

doi:10.1002/eji.200737418

Cited by 26 publications

(19 citation statements)

References 15 publications

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“…null T cells have suggested that they are related to NK cells and represent a population of NK-like T cells [29]. In support of this hypothesis, we found that CD4 +…”

Section: Cd28supporting

confidence: 87%

T cell senescence and contraction of T cell repertoire diversity in patients with chronic obstructive pulmonary disease

Lambers¹,

Hacker²,

Posch

et al. 2009

Clinical and Experimental Immunology

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SummaryPathogenetic mechanisms leading to chronic obstructive pulmonary disease (COPD) remain poorly understood. Natural killer (NK)-like T cell receptors (CD94, 158) and intracellular perforin, granzyme B were increased in CD4+ CD28 null cells. Cytokine production after triggering of peripheral blood mononuclear cells (PBMCs) was elevated in patients at early disease stages. Receiver operating characteristic curve plotting revealed that presence of CD4 + CD28 null T cells has a diagnostic value. These CD4 + CD28 null T cells show increased expression of NK-like T cell receptors (CD94, 158) and intracellular perforin and granzyme B. Furthermore, triggering of PBMCs obtained from patients with mild COPD led to increased interferon-g and tumour necrosis factor-a production in vitro compared with controls. Our finding of increased CD4 + CD28 null T cells in COPD indicates that chronic antigen exposure, e.g. through contents of smoke, leads to loss of CD28 and up-regulation of NK cell receptors expression on T cells in susceptible patients.

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“…null T cells have suggested that they are related to NK cells and represent a population of NK-like T cells [29]. In support of this hypothesis, we found that CD4 +…”

Section: Cd28supporting

confidence: 87%

T cell senescence and contraction of T cell repertoire diversity in patients with chronic obstructive pulmonary disease

Lambers¹,

Hacker²,

Posch

et al. 2009

Clinical and Experimental Immunology

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“…Unlike naive T cells, effector memory CD8 T cells commonly express receptors originally found on natural killer (NK) cells, and therefore are often referred to as NK receptors. [5][6][7][8][9] Among these are members of the leukocyte receptor complex (LRC)-encoded killer cell immunoglobulin like receptors (KIR) as well as members of the natural killer gene complex (NKC)-encoded C-type lectin-like receptors (CTLR). [7][8][9] Examples of NKC-encoded CTLR expressed on T cells are mouse Ly49 family MHC class I receptors and killer lectin-like receptor (KLR) family members such as CD94/NKG2A and KLRG1.…”

Section: Introductionmentioning

confidence: 99%

NKp80 defines and stimulates a reactive subset of CD8 T cells

Kuttruff

Koch

Kelp

et al. 2009

Blood

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NKp80, an activating homodimeric C-type lectin-like receptor (CTLR), is expressed on essentially all human natural killer (NK) cells and stimulates their cytotoxicity and cytokine release. Recently, we demonstrated that the ligand for NKp80 is the myeloid-specific CTLR activation-induced C-type lectin (AICL), which is encoded in the natural killer gene complex (NKC) adjacent to NKp80. Here, we show that NKp80 also is expressed on a minor fraction of human CD8 T cells that exhibit a high responsiveness and an effector memory phenotype. Gene expression profiling and flow cytometric analyses revealed that this NKp80(+) T-cell subset is characterized by the coexpression of other NK receptors and increased levels of cytotoxic effector molecules and adhesion molecules mediating access to sites of inflammation. NKp80 ligation augmented CD3-stimulated degranulation and interferon (IFN)gamma secretion by effector memory T cells. Furthermore, engagement of NKp80 by AICL-expressing transfectants or macrophages markedly enhanced CD8 T-cell responses in alloreactive settings. Collectively, our data demonstrate that NKp80 is expressed on a highly responsive subset of effector memory CD8 T cells with an inflammatory NK-like phenotype and promotes T-cell responses toward AICL-expressing cells. Hence, NKp80 may enable effector memory CD8 T cells to interact functionally with cells of myeloid origin at sites of inflammation.

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“…Such immunophenotypic sharing by NK and T cells blurs the distinction between these cell types. 3,4 Analysis of T-cell receptor gene (TCR) rearrangements is the gold standard to distinguish T from NK cells. The productive rearrangement of the TCR gene in mature T cells distinguishes the two cell types unambiguously.…”

mentioning

confidence: 99%

“…The productive rearrangement of the TCR gene in mature T cells distinguishes the two cell types unambiguously. 4 TCR gene rearrangement analysis using Southern blot hybridization or nested polymerase chain reaction (PCR) analyses disclosed variable T-cell clonality in ENKTLs ranging from 0 to 27%. 5,6 The BIOMED-2 Concerted Action protocol using multiplex PCR primers has now replaced conventional PCR in assaying gene rearrangements and has higher sensitivity than conventional PCR analyses that use fewer primer sets.…”

mentioning

confidence: 99%

Nasal-type NK/T-cell lymphomas are more frequently T rather than NK lineage based on T-cell receptor gene, RNA, and protein studies: lineage does not predict clinical behavior

et al. 2016

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Extranodal natural killer (NK)/T-cell lymphoma (ENKTL), nasal type, comprises NK or cytotoxic T cells. We evaluated the clinical impact of cell type and the usefulness of T-cell receptor (TCR) gene transcripts in distinguishing cell lineage. One hundred and eight cases of ENKTL were analyzed for TCR gene rearrangements using the BIOMED-2 protocol and for TCR gene expression using immunohistochemistry for TCR-βF1 and TCR-cγM1, and RNA in situ hybridization for TCR gene transcripts. Prognostic factors were analyzed. Among the 108 cases, 44 were monoclonal for a TCR rearrangement (40%) while 64 (60%) were undefinable. The monoclonal cases expressed TCR-βF1 in 14 out of 40 cases (35%) and TCR-cγM1 in 1 out of 44 cases (2%). The 64 undetermined cases expressed TCR-βF1 in 15 cases (23%) and TCR-cγM1 in 1 (2%). Thirteen of 40 TCR-β constant gene transcript-positive cases (33%) expressed TCR-βF1 and one of nine TCR-γ constant gene transcript-positive cases (11%) expressed TCR-cγM1. TCR gene transcripts were not useful in the distinction of cell lineages. TCR gene transcripts were positive in ENKTLs as well as in normal B cells and aggressive NK-cell leukemia. Based on gene rearrangements and immunohistochemistry for TCR, there were 60 T-cell type cases (56%), 32 NK-cell type cases (30%), and 16 cases with an undetermined cell type (14%). TCR protein was expressed in 30/60 T-ENKTLs (50%) in a variable fraction of tumor cells. There were no significant differences in clinical findings or overall patient survival between T-or NK-cell types of ENKTL, although those with a T-cell type tended to show a better prognosis for those with localized nasal lymphomas. Univariate and multivariate analysis showed that a non-nasal ENKTL, age 460 years, high level of lactate dehydrogenase, bone marrow involvement, and the absence of radiotherapy were independent prognostic factors.

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Back to the future –defining NK cells and T cells

Cited by 26 publications

References 15 publications

T cell senescence and contraction of T cell repertoire diversity in patients with chronic obstructive pulmonary disease

T cell senescence and contraction of T cell repertoire diversity in patients with chronic obstructive pulmonary disease

NKp80 defines and stimulates a reactive subset of CD8 T cells

Nasal-type NK/T-cell lymphomas are more frequently T rather than NK lineage based on T-cell receptor gene, RNA, and protein studies: lineage does not predict clinical behavior

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