Natural killer T cells in families of patients with systemic lupus erythematosus: Their possible role in regulation of IGG production

Green, Matthew R. J.; Kennell, Amy S. M.; Larché, Maggie; Seifert, Martin; Isenberg, David; Salaman, Myer R.

doi:10.1002/art.22326

Cited by 50 publications

(47 citation statements)

References 25 publications

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“…In our study, we observed an elevated frequency of CD56 + T cells in the peripheral blood of fingolimod-treated MS patients. Our patients did not have malignancy, CD56 upregulation was not consistently reported in autoimmune diseases, including nF-MS patients in this study35414243. Thus, the association between infectious pathogens and CD56 upregulation is of particular interest.…”

Section: Discussionmentioning

confidence: 56%

Altered T cell phenotypes associated with clinical relapse of multiple sclerosis patients receiving fingolimod therapy

Fujii

Kondo

Ochi

et al. 2016

Sci Rep

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Multiple sclerosis (MS) is a T cell-mediated autoimmune disease. Fingolimod, a highly effective disease-modifying drug for MS, retains CCR7+ central memory T cells in which autoaggressive T cells putatively exist, in secondary lymphoid organs, although relapse may still occur in some patients. Here, we analyzed the T cell phenotypes of fingolimod-treated, fingolimod-untreated patients, and healthy subjects. The frequency of CD56+ T cells and granzyme B-, perforin-, and Fas ligand-positive T cells significantly increased during fingolimod treatment. Each T cell subpopulation further increased during relapse. Interestingly, T cells from fingolimod-treated patients exhibited interferon-γ biased production, and more myelin basic protein-reactive cells was noted in CD56+ than in CD56− T cells. It is likely that the altered T cell phenotypes play a role in MS relapse in fingolimod-treated patients. Further clinical studies are necessary to investigate whether altered T cell phenotypes are a biomarker for relapse under fingolimod therapy.

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Section: Discussionmentioning

confidence: 56%

Altered T cell phenotypes associated with clinical relapse of multiple sclerosis patients receiving fingolimod therapy

Fujii

Kondo

Ochi

et al. 2016

Sci Rep

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“…Although the results presented here offer no direct evidence about the mechanisms by which this pattern occurs, the data are consistent with the existence of a regulatory system that constrains the maximum total level of these two cell types to 30% and permits shifts in the balance between them. Both activated T helper cells and activated NK cells exhibit signs of being important to SLE pathology [16], [22]–[25], even at the transcriptional level [26]. Perhaps their relative levels define clinically important subtypes of SLE, and if so they might be useful diagnostic markers for this disease characteristic.…”

Section: Discussionmentioning

confidence: 99%

“…Some of these differences are changes in the abundance of specific leukocyte populations [16], [17], suggesting that systematic large-scale characterization of the cellular composition of SLE patient blood would measure quantitative differences relevant to the disease pathophysiology. Here we use microarray deconvolution to explore immune cell subsets and activation states in SLE patient blood.…”

Section: Introductionmentioning

confidence: 99%

Deconvolution of Blood Microarray Data Identifies Cellular Activation Patterns in Systemic Lupus Erythematosus

Abbas¹,

Wolslegel²,

Seshasayee³

et al. 2009

PLoS ONE

399

509

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Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease with a complex spectrum of cellular and molecular characteristics including several dramatic changes in the populations of peripheral leukocytes. These changes include general leukopenia, activation of B and T cells, and maturation of granulocytes. The manifestation of SLE in peripheral blood is central to the disease but is incompletely understood. A technique for rigorously characterizing changes in mixed populations of cells, microarray expression deconvolution, has been applied to several areas of biology but not to SLE or to blood. Here we demonstrate that microarray expression deconvolution accurately quantifies the constituents of real blood samples and mixtures of immune-derived cell lines. We characterize a broad spectrum of peripheral leukocyte cell types and states in SLE to uncover novel patterns including: specific activation of NK and T helper lymphocytes, relationships of these patterns to each other, and correlations to clinical variables and measures. The expansion and activation of monocytes, NK cells, and T helper cells in SLE at least partly underlie this disease's prominent interferon signature. These and other patterns of leukocyte dynamics uncovered here correlate with disease severity and treatment, suggest potential new treatments, and extend our understanding of lupus pathology as a complex autoimmune disease involving many arms of the immune system.

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“…NKT-like cells were reported to be decreased in SLE patients. The number of NKT-like cells correlated inversely with SLE disease activity [13]. …”

Section: Introductionmentioning

confidence: 99%

Effect of Interleukin-15 on CD11b, CD54, and CD62L Expression on Natural Killer Cell and Natural Killer T-Like Cells in Systemic Lupus Erythematosus

Lin

Chen

Kuo

et al. 2016

Mediators of Inflammation

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Adhesion molecules may play an important role in systemic lupus erythematosus (SLE) pathogenesis. We investigated the effect of interleukin- (IL-) 15 on CD11b, CD54, and CD62L expression on natural killer (NK) cells, T cells, and CD56+CD3+ NKT-like cells from SLE subjects and healthy controls. SLE patients had decreased circulating NK cells and NKT-like cells compared to controls. NK cells from SLE patients showed higher CD11b and CD62L expression compared to controls. IL-15 enhanced CD11b and CD54 but downregulated CD62L expression on NK cells from SLE patients. Similar observations were found for T cells and NKT-like cells. NK cells from SLE patients expressed higher CD56 than controls; both could be further enhanced by IL-15. IL-15 also enhanced CD56 expression of NKT-like cells from SLE patients. A greater degree of IL-15 induced downregulation of CD62L on NKT-like cells noted in SLE patients compared to controls. The percentage of CD11b expressing NK cells and the % inhibition of CD62L expression on NKT-like cells by IL-15 correlated with serum anti-dsDNA levels in SLE patients, respectively. Taken together, we demonstrated the dysfunctional NK and NKT-like cells in SLE patients with regard to CD11b and CD62L expression and their response to IL-15.

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Natural killer T cells in families of patients with systemic lupus erythematosus: Their possible role in regulation of IGG production

Cited by 50 publications

References 25 publications

Altered T cell phenotypes associated with clinical relapse of multiple sclerosis patients receiving fingolimod therapy

Altered T cell phenotypes associated with clinical relapse of multiple sclerosis patients receiving fingolimod therapy

Deconvolution of Blood Microarray Data Identifies Cellular Activation Patterns in Systemic Lupus Erythematosus

Effect of Interleukin-15 on CD11b, CD54, and CD62L Expression on Natural Killer Cell and Natural Killer T-Like Cells in Systemic Lupus Erythematosus

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